ArticlePDF AvailableLiterature Review

Abstract and Figures

Spices and herbs have been in use for centuries both for culinary and medicinal purposes. Spices not only enhance the flavor, aroma, and color of food and beverages, but they can also protect from acute and chronic diseases. More Americans are considering the use of spices and herbs for medicinal and therapeutic/remedy use, especially for various chronic conditions. There is now ample evidence that spices and herbs possess antioxidant, anti-inflammatory, antitumorigenic, anticarcinogenic, and glucose- and cholesterol-lowering activities as well as properties that affect cognition and mood. Research over the past decade has reported on the diverse range of health properties that they possess via their bioactive constituents, including sulfur-containing compounds, tannins, alkaloids, phenolic diterpenes, and vitamins, especially flavonoids and polyphenols. Spices and herbs such as clove, rosemary, sage, oregano, and cinnamon are excellent sources of antioxidants with their high content of phenolic compounds. It is evident that frequent consumption of spicy foods was also linked to a lower risk of death from cancer and ischemic heart and respiratory system diseases. However, the actual role of spices and herbs in the maintenance of health, specifically with regards to protecting against the development of chronic, noncommunicable diseases, is currently unclear. This review highlights potential health benefits of commonly used spices and herbs such as chili pepper, cinnamon, ginger, black pepper, turmeric, fenugreek, rosemary, and garlic.
Content may be subject to copyright.
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 395
Spices and herbs have been in use for centuries
both for culinary and medicinal purposes. Spices
not only enhance the avor, aroma, and color of
food and beverages, but they can also protect
from acute and chronic diseases. More Americans
are considering the use of spices and herbs for
medicinal and therapeutic/remedy use, especially
for various chronic conditions. There is now
ample evidence that spices and herbs possess
antioxidant, anti-inammatory, antitumorigenic,
anticarcinogenic, and glucose- and cholesterol-
lowering activities as well as properties that
affect cognition and mood. Research over the
past decade has reported on the diverse range
of health properties that they possess via their
bioactive constituents, including sulfur-containing
compounds, tannins, alkaloids, phenolic
diterpenes, and vitamins, especially avonoids
and polyphenols. Spices and herbs such as clove,
rosemary, sage, oregano, and cinnamon are
excellent sources of antioxidants with their high
content of phenolic compounds. It is evident that
frequent consumption of spicy foods was also
linked to a lower risk of death from cancer and
ischemic heart and respiratory system diseases.
However, the actual role of spices and herbs in the
maintenance of health, specically with regards
to protecting against the development of chronic,
noncommunicable diseases, is currently unclear.
This review highlights potential health benets of
commonly used spices and herbs such as chili
pepper, cinnamon, ginger, black pepper, turmeric,
fenugreek, rosemary, and garlic.
Spices have been an integral part of culinary culture
around the world and have a long history of use for
avoring, coloring, and preserving food, as well as for
medicinal purposes. The increased use of spices as avorings
in foods is a major trend worldwide (1). Spices not only
enhance the avor, aroma, and color of food and beverages,
but they may also protect against the development of acute
and chronic, noncommunicable diseases and help people
maintain health. The long historical use of herbs and spices
Health Benets of Culinary Herbs and Spices
T. AlAn JiAng
Nouritek International LLC, Timonium, MD 21093
for their medicinal benets is fully acknowledged, and there
is a growing amount of literature concerning the potential/
purported benets of these foods from a health perspective.
These benets include their possible role in conferring
protection against cardiovascular and neurodegenerative
diseases, cardiovascular disease, cancer, and type 2 diabetes
mellitus (T2DM; 1–3).
Spices and herbs have been extensively studied in different
countries because of their benecial effects on human health
(1, 4). However, the interest in spices has only recently grown
in the Western world (5, 6). Greater awareness of ethnic spices
for disease prevention and health promotion is needed in this
Use and Knowledge of Spices and Herbals
The U.S. Department of Agriculture reports that the
consumption of spices in the United States has climbed
exponentially over the course of the last half-century, with spices
such as ginger and chili pepper being used more frequently than
ever before (6). According to the U.S. National Health and
Nutrition Examination Survey, 5–10% of adults in the United
States use botanical supplements such as spices, for health
benets (7, 8). Such increased use could in part be because of
the lack of side effects from spices, greater availability than
traditional medicines, and the consideration of known health
benets of spices (6–8).
It is evident that more Americans are considering the use of
spices and herbs for medicinal and therapeutic uses, especially
to remedy various chronic conditions, reduce disease symptoms,
and aid in treatment and management of common health
problems. A recent cross-sectional survey study involving 703
adults in the Midwestern United States examined consumers’
perceptions about spices and their use and predictors of spice
use (9) found that almost half of the participants were interested
in learning about health benets of spices (48%) and were
willing to use spices as complementary and alternative medicine
therapies (51%). Most (>50%) of the participants were familiar
with or had used 8 out of the 10 listed spices. The majority
of participants (54%) was currently using one or more spices
on a daily basis and believed that ginger (64%), garlic (58%),
and cinnamon (56%) could promote good health and wellness
(Table 1). Furthermore, the majority of the participants listed
7 out of 10 spices as effective in preventing a specic disease
with ginger (72%), garlic (68%), and cinnamon (67%) listed as
effective by more than two-thirds of the participants. In addition
to the adult population use, spices have also been explored
in pediatric populations. For example, more than 1/10 of the
infants and children were given spices, primarily to remedy
minor ailments such as fussiness or stomach complications,
coughs, and colds.
Guest edited as a special report on “Authentication, Quality,
Health, and Regulation of Spices and Herbs” by Paul Ford and Milda
Corresponding author’s e-mail:
396 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
foods almost every day had a relative 14% lower risk of death
compared with those who consumed spicy foods less than once a
week. It was found that frequent consumption of spicy foods was
also linked to a lower risk of death from cancer, ischemic heart
diseases, and respiratory diseases, and this was more evident in
women than in men. People who consumed fresh chili tended to
have a lower risk of death from cancer, ischemic heart disease,
and diabetes (16, 17).
In addition, subjects with a high spice preference had a lower
salt intake and blood pressure than subjects who disliked spicy
food. The enjoyment of spicy avors enhanced salt sensitivity
and reduced salt preference. Salt intake and salt preference
were related to the regional metabolic activity in the insula
and orbitofrontal cortex (OFC) of participants. A more recent
multicenter, double-blind observational and interventional
study showed that administration of capsaicin, the major spicy
component of chili pepper, enhanced the insula and OFC
metabolic activity in response to high-salt stimuli, which reversed
the salt intensity-dependent differences in the metabolism of
the insula and OFC (18). It was concluded that enjoyment of
spicy foods may signicantly reduce individual salt preference,
daily salt intake, and blood pressure by modifying the neural
processing of salty taste in the brain. Application of spicy avor
may be a promising behavioral intervention for reducing high
salt intake and blood pressure.
Overview of Selected Herbs and Spices
Chili Pepper
Bioactive components.—Red pepper contains 0.2–2%
capsaicinoids, which are responsible for the pungency or bite in
capsicums. Capsaicin, an alkaloid, accounts for about 50–70%
of the total capsacinoids and dihydrocapasaicin for 20–25%,
which, together with capasaicin, provides the eriest notes from
midpalate to throat. Red pepper also contains newly discovered,
nonpungent compounds called capsinoids (e.g., capsiate and
The benecial effects of red pepper have long been
documented. The habitual consumption of spicy foods was
inversely associated with total and certain cause-specic
mortality (cancer, ischemic heart diseases, and respiratory
diseases), independent of other risk factors of death. A
recent large population-based prospective study analyzed
the association between consumption of hot red chili peppers
and mortality, using a population-based prospective cohort
from the National Health and Nutritional Examination Survey
III. The frequency of hot red chili pepper consumption was
measured in 16 179 participants at least 18 years of age. Total
and cause-specic mortality were the main outcome measures.
Total mortality for participants who consumed hot red chili
peppers was 21.6% compared with 33.6% for those who did
not (absolute risk reduction of 12%; relative risk of 0.64).
Consumption of hot red chili peppers was associated with
a 13% reduction in the instantaneous hazard of death. It is
documented that the consumption of hot red chili pepper was
associated with reduced mortality. The ndings are in line with
previous evidence showing potential protective effects of spicy
foods on human health (16).
Antioxidant anti-inammatory effects.—Red pepper capsaicin
has antioxidant potential in mitigating oxidative stress in various
tissues or organs in both in vitro and animal models (19–21).
Biological Activities of Spices and Herbs Constituents
Culinary herbs and spices are foods that are a rich source
of bioactive molecules such as sulfur-containing compounds,
tannins, alkaloids, phenolic diterpenes, and vitamins, especially
avonoids and polyphenols (4, 10). Spices and herbs such as
clove, rosemary, sage, oregano, and cinnamon are excellent
sources of antioxidants with their high content of phenolic
compounds (10, 11).
Research over the past decade has reported that bioactive
constituents of spices possess the diverse range of health benets
(1, 5, 11, 12). There is now ample evidence that culinary herbs
and spices are sources of constituents that possess antioxidative,
anti-inammatory, antitumourigenic, anticarcinogenic, and
glucose- and cholesterol-lowering activities as well as properties
that affect cognition and mood, which are actively used in
preclinical, clinical, and therapeutic trials investigating new
treatments of diseases. In addition, there is now a growing
amount of literature on how polyphenols confer health benets
via their action on gut microbiota (13, 14), which, in humans,
have been recently related to risks of diabetes, cardiovascular
disease, liver cirrhosis, etc.
Effect of Spices on Human Health
Culinary herbs and spices have been reported to have various
benecial effects on human health. There is ample research
evidence to suggest that spice consumption is particularly related
to the reduced risk of mortality as a result of cancer, ischemic
heart diseases, and respiratory diseases. A recent observational
study assessed consumption of spicy foods as part of a daily diet
and the total risk and causes of death in 487 375 participants, aged
30–79 years, during a median follow-up of 7.2 years in China
and concluded that people eat spicy food to improve health (15).
Compared with participants who ate spicy foods less than once a
week, those who consumed spicy foods 1 or 2 days a week were
at a 10% reduced risk of death (hazard ratios for death was 0.90).
And those who ate spicy foods three to ve and six to seven days
a week were at a 14% reduced risk of death (the hazard ratios for
death were both 0.86). In other words, participants who ate spicy
Table 1. Perceived efcacy of spices in promoting health
and wellness (9)
Effective na
(%b agreement)
Ginger 450 (64)
Garlic 404 (58)
Cinnamon 392 (56)
Chili pepper 300 (43)
Turmeric 251 (36)
Cilantro 168 (24)
Cloves 163 (23)
Black pepper 163 (23)
Curry leaves 108 (15)
Fenugreek 76 (11)
a n = 703.
b % = Percent of individuals who believe that a certain spice can
promote health and wellness.
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 397
red pepper (C. annum; CH-19 sweet, a nonpungent cultivar of
red pepper, containing capsiate at 0.1 mg/kg dry weight) could
enhance thermogenesis but have no impact on blood pressure
and heart rate (47, 48). A 12 week placebo-controlled human
trial conrmed that consumption of capsinoids from C. annum
was associated with abdominal fat loss (49). Furthermore,
Janssens et al. (50) investigated the 24 h effects of capsaicin
on energy expenditure, substrate oxidation, and blood pressure
during 25% negative energy balance and found that consuming
2.56 mg capsaicin per meal supports negative energy balance
by counteracting the unfavorable negative energy balance effect
of decrease in components of energy expenditure as well as
promotes fat oxidation in negative energy balance.
Gut health.—Evidence suggests capsaicin is a gastroprotective
agent in peptic ulcer disease (51, 52). Capsaicin inhibits
acid secretion and stimulates alkali and mucus secretions
(particularly gastric mucosal blood ow), which help in the
prevention and healing of ulcers (53). Red pepper sauce (which
is high in capsaicin) helps with issues swallowing by increasing
the contractility and motility response of the human esophagus.
An acute administration of capsaicin seems to improve the
motor performance of the esophageal body in patients with
ineffective esophagus motility (54).
The antimicrobial activity of spices, has been highlighted
by inhibitory effects against Helicobacter pylori and other
bacteria and fungi (55, 56). Chili pepper has long been
recognized to have a benecial effect on the gut microbiota
in humans. In recent years, rapidly emerging evidence has
implicated gut microbiota as a novel and important metabolic
factor that affects the health of the host (57), and several
studies in humans have related abundance, composition,
and metabolites of gut microbiota to risk of obesity (58, 59),
diabetes (60), liver cirrhosis (61), and cardiovascular disease
(62). In a 6 week, controlled feeding trial, subjects were given
the weight maintenance diet sequentially contained with
up to 10 mg/day capsaicin from chili powder (63). Dietary
capsaicin increased the Firmicutes:Bacteroidetes ratio and
Faecalibacterium abundance, accompanied with increased
plasma levels of glucagon-like peptide 1 (GLP-1) and gastric
inhibitory polypeptide and decreased plasma ghrelin level.
Further enterotype analysis revealed that these subjects could
be clustered into Bacteroides enterotype (E1) and Prevotella
enterotype (E2), and the above benecial effects were
mainly obtained in E1 subjects. Moreover, E1 subjects had
signicantly higher fecal Faecalibacterium abundance and
butyrate concentration after capsaicin interventions than those
in E2 subjects.
Bioactive components.—Cinnamon’s key components are
essential oils and other derivatives such cinnamaldehyde,
cinnamic acid and cinnamate (bark oil; 60–80%), eugenol
(leaf oil; 10%), and water soluble polyphenols (4–10%), e.g.,
catechin, epicatechin, procyanidin, quercetin, kaempferol,
and polyphenolic polymers. The avonoids are primarily
proanthocyanidins and oligomers of cinnamtannins. The doubly
linked phenol type A polymers are believed to be the bioactive
component for glucose metabolism (64).
Antibacterial and antifungal activity.—Extracts of cinnamon
and its major components, cinnamaldehyde and eugenol, have
Capsaicin-inhibited neutrophil (inammatory cells) migration
toward the inammatory focus reduced vascular permeability and
proinammatory cytokine production in an animal study (21).
Capsaicin may also suppress obesity-induced inammation by
modulating messenger molecules released by obese mice fat cells
and inactivating macrophage to release proinammatory mediators
in vitro (22).
Cardiovascular health.—The antioxidant and antiplatelet
properties of capsaicin and the important role of capsaicin in
regulating energy metabolism may also contribute to its benecial
effects on the cardiovascular system (23–26). An animal study
showed that 3 mg/kg/day capsaicin reduced low-density
lipoprotein (LDL) levels, increased high-density lipoprotein
(HDL) levels, and reduced oxidative stress levels measured as
malondialdehyde in various tissues (27). In another animal study,
when capsaicin was used alone (0.015% in the diet) or combined
with curcumin, dietary high-fat–induced excess of triglycerides
in the blood was countered by 14 and 12%, respectively; the
total cholesterol was reduced 23 and 21%, respectively (28).
In addition, capsaicin preferentially inhibited arachidonic acid-
induced platelet aggregation in vitro (29). Capsaicin may also
defend against heart disease via a transient receptor potential
(TRP)-mediated modulation of coronary blood ow (30). Two
randomized crossover intervention studies revealed 4 weeks of
regular consumption of a chili blend (55% cayenne chili) at 16 g
a day increased the resistance of serum lipoproteins to oxidation
and reduced resting heart rate. It also increased effective
myocardial perfusion pressure time in men but not women
(31, 32). A randomized, double-blind, placebo-controlled trial in
44 pregnant women with gestational DM (GDM) documented
that capsaicin-containing chili supplementation (5 mg/day
capsaicin) regularly improved postprandial hyperglycemia and
hyperinsulinemia as well as fasting lipid metabolic disorders in
women with GDM, and it decreased the incidence of large-for-
gestational-age newborns (33).
Blood glucose control.—Human trials found that 5 g or
more of chili pepper (Capsicum frutescens) was associated
with a decrease in blood glucose level and maintenance of
healthy insulin levels (34–36). Animal studies suggested that
red pepper may affect insulin secretion from beta-cells and/or
peripheral insulin resistance, reduce liver glucose output and
increase glycogen (the main form of body fuel) storage, as well
as activate the peroxisome proliferator-activated receptors in
vitro, which involve cell glucose and fat metabolism (37–39).
Furthermore, dietary capsaicin may provide benecial effects
on glucose homeostasis via activating the TRP vanilloid type 1
(TRPV1; 40).
Thermogenesis, satiety, and weight management.—Short-
term consumption of red pepper may have the potential to
assist in body weight management by increasing satiety and
fullness, reducing energy and fat intake, increasing body heat
production (thermogenesis), raising the body’s metabolic rate
(41–43), preventing fat cells from growing into mature cells
(adipogenesis; 44), and increasing the rate of fat burn-off (fat
oxidation; 45). TRP channels, which are primary receptors for
pungent agents such as capsaicin, may in part be responsible
for lipid catabolism and thermogenesis; activating of TRPV1
appears to stimulate cellular mechanisms against obesity (40).
Human studies suggest that red pepper enhances
thermogenesis and fat oxidation but also affect blood pressure
and heart rate (45–47). The longer-term use of capsaicin may be
also limited by its strong pungency. However, a certain type of
398 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
hypoglycemic medications and other lifestyle therapies had
modest effects on FPG and HbA1c (81).
Proanthyocyanidins are considered active ingredients in
cinnamon aqueous extracts. Preclinical animal studies provide
evidence that components of cinnamon may decrease blood
glucose levels and increase insulin sensitivity (85). Cinnam-
aldehyde is another active component derived from cinnamon.
Accumulating evidence supports the notion that cinnamaldehyde
exhibits blood glucose-lowering effects in diabetic animals
by increasing glucose uptake and improving insulin sensitivity
in adipose and skeletal muscle tissues, improving glycogen
synthesis in liver, restoring pancreatic islets dysfunction,
slowing gastric emptying rates, and improving diabetic renal
and brain disorders (86). Cinnamaldehyde exerts these effects
through its action on multiple signaling pathways, including
JNK/p38MAPK, TRPA1-ghrelin, and Nrf2 pathways (87).
Additionally, obese mice fed for 5 weeks with a cinnamon-
containing diet signicantly reduced their cumulative body
weight gain and improved glucose tolerance without detectable
modication of insulin secretion (87).
Although evidence of glucose control in humans is
inconsistent, there is evidence of dose-related hypoglycemic
effects. Recent human studies showed that cinnamon
supplements of 3 g/day or more had improved glucose control
and insulin sensitivity in both healthy and diabetic subjects
(88–92). In addition, consuming 500 mg/day aqueous extract of
cinnamon (approximately 10 g cinnamon ground powder/day)
for 12 weeks led to improvements in several metabolic features
(i.e., fasting blood sugar, SBP, and body composition; 93).
However, most human studies did not show any improvements
in blood glucose control or insulin sensitivity when cinnamon
was used at <3 g/day doses (92, 94–97).
Hepatoprotective effect.—One study found the ethanol
extract of cinnamon showed hepatoprotective action against
carbon tetrachloride–induced lipid peroxidation and liver
injury in rats by elevating antioxidant enzyme activities (98).
Cinnamon bark extract reduced the hepatic lipid accumulation
and protected the liver from acute alcohol-induced fatty liver in
mice (99).
Neuroprotective property.—Various cinnamon species
and their biologically active ingredients have renewed
the interest toward the treatment of patients with mild-to-
moderate Alzheimer’s disease (AD) through the inhibition of
tau protein aggregation and the prevention of the formation
and accumulation of amyloid-β (Abeta) peptides into the
neurotoxic oligomeric inclusions, both of which are considered
to be the AD trademarks. An aqueous extract of cinnamon
inhibits tau protein activity (a protein that becomes toxic
when it accumulates and twists inside nerve cells in the
brain), and Abeta insult of neuronal cells in an in vitro model
(100, 101). Indeed, cinnamon possesses neuroprotective
effects by interfering with multiple oxidative stress and
proinammatory pathways. Additionally, cinnamon modulates
endothelial functions and attenuates the vascular cell adhesion
molecules. Cinnamon polyphenols may induce AD epigenetic
modications. Cinnamon, particularly cinnamaldehyde, seems
to be effective and safe approaches for treatment and prevention
of AD onset and/or progression. However, further molecular
and translational research studies as well as prolonged clinical
trials are required to establish the therapeutic safety and
efcacy in different Cinnamon spp.
been shown to attack major respiratory and gastrointestinal tract
pathogens in vitro (65, 66). An anecdotal report suggests that
cinnamon may have benecial effects on chronic salmonella
infection (67). Further, an in vitro study suggested cinnamon
may have some bactericidal activity against H. pylori (68), but
there is a lack of evidence to support the use of cinnamon for
H. pylori infection eradication in humans.
Anti-inammatory and antioxidant effects.—Cinnamon
polyphenol extract suppressed inammation processes through
the regulation of anti- and proinammatory gene expression
in vitro (69, 70). Cinnamaldehyde-inhibited cyclooxygenase-2
(COX-2) and inducible nitric oxide synthase (iNOS), two major
inammation systems (70). In a double-blind, placebo-controlled
trial involving 22 overweight subjects with impaired fasting
blood glucose, 500 mg/day aqueous extract of cinnamon (high
in type A polyphenols) for 12 weeks reduced oxidative stress as
measured by plasma malondialdehyde (MDA) levels (71).
Cardiovascular health.—Cinnamon and cinnamon extract
(high in type A polyphenols) lowered sugar-induced blood
pressure increase in one study with rats predisposed to
hypertension (72). Cinnamaldehyde has been reported to
inhibit platelet aggregation in vitro in human and rabbit cells
as well as reduce blood clots formed within a blood vessel in
an animal study (73). By regulating gene expression involving
inammatory, insulin, and lipoprotein metabolism signaling
pathways, a cinnamon extract (high in type A polyphenols)
inhibited the overproduction of lipoproteins and serum
triglycerides after a meal, suggesting that this extract may
be benecial in the control of lipid metabolism (74–76). In a
recent systematic review and meta-analysis, Maierean et al. (77)
assessed 13 randomized controlled trials with 750 participants
investigating the effect of cinnamon supplementation on blood
lipid concentrations. Cinnamon supplementation signicantly
reduced blood triglycerides and total cholesterol concentrations
without any signicant effect on LDL-cholesrterol (LDL-C)
and HDL-cholesterol (HDL-C). Moreover, cinnamon may have
protective effects against metabolic syndrome aspects in various
ways, and the use of cinnamon can be effective in reducing
metabolic syndrome complications (78, 79). Consumption of
cinnamon (short term) is associated with notable reductions
in systolic blood pressure (SBP) and diastolic blood pressure
(DBP; 80).
Blood glucose control.—The consumption of cinnamon is
associated with a statistically signicant decrease in fasting
plasma glucose (FPG) levels. Cinnamon thus has been suggested
to help patients with T2DM achieve better glycemic control,
although conclusions from meta-analyses are mixed (81–84).
Eleven randomized, controlled trials that met the inclusion
criteria were identied and enrolled 694 adults with T2DM both
receiving and not receiving hypoglycemic medications. In 10 of
the studies, participants continued to take their hypoglycemic
medications during the cinnamon intervention period. The
studies ranged from 4 to 16 weeks in duration, and 7 of
the studies were double-blind. Cinnamon doses ranged from
120 to 6000 mg/day. All 11 of the studies reported some
reductions in FPG during the cinnamon intervention, and of
the studies measuring hemoglobin A1c (HbA1c), very modest
decreases were also apparent with cinnamon, whereas changes
in the placebo groups were minimal. However, only four
studies achieved the American Diabetes Association treatment
goals [FPG < 7.2 mmol/L (130 mg/dL) and/or HbAlc <7.0].
It was concluded that cinnamon supplements added to standard
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 399
recovery following intense exercise in a randomized trial on
20 nonweight-trained participants (128).
Antiglycation and antiglycemic effects.—The accumulation
of advanced glycation endproducts (AGEs) as a result of
nonenzymatic reaction betweem proteins and sugar has been
implicated in unhealthy conditions associated with aging and
diabetes. Thus, inhibiting AGEs formation is believed to play a
role in the prevention of diabetic complications. In vitro studies
showed ginger extract could prevent and/or inhibit protein
glycation (129, 130). Animal data also indicated a hypoglycemic
effect for ginger extract (131–134). In randomized clinical
trials, it was found that supplementation of ginger (1.6–3.0 g
daily) improved insulin sensitivity and some fractions of lipid
proleand reduced C-reactive protein (CRP) and prostaglandin E2
in type 2 diabetic patients. Glycemic indexes (lowering blood
glucose and HbA1c), insulin sensitivity, and lipid prole, as well
as total antioxidant capacity, MDA, CRP, and paraoxonase-1
activity were improved in patients with T2D (135–137).
Weight management potential.—It is evident that oral
ingestion of ginger could induce thermoregulatory function
and fat oxidation in humans. Serum levels of free fatty acids
were signicantly elevated at 120 min after intake of 1.0 g
dried ginger root powder in both the morning and afternoon.
Morning ginger intake also signicantly reduced respiratory
exchange ratios and elevated fat oxidation by 13.5% 120 min
after ingestion. These results suggest that the effect of a single
oral ginger administration facilitate fat use (138). Mansour
et al. (139) measured resting state energy expenditure for 6 h
after consumption of a breakfast meal with or without 2 g
ginger powder dissolved in a hot-water beverage. There was
a signicant effect of ginger on thermic effect of food (ginger
versus control = 42.7 ± 21.4 kcal/day, P = 0.049). Visual
analog scale ratings showed lower hunger (P = 0.002), lower
prospective food intake (P = 0.004), and greater fullness
(P = 0.064) levels with ginger consumption versus the
control. These results, which show enhanced thermogenesis
and reduced feelings of hunger with ginger consumption,
suggest a potential role of ginger in weight management.
Furthermore, ginger consumption (2 g/day ginger powder)
for 12 weeks in obese women showed a signicant decrease
in body mass index (BMI), serum insulin and homeostatic
model assessment–insulin resistance (HOMA-IR) index, and
total appetite score, demonstrating a minor benecial effect
of ginger supplementation on weight loss and some metabolic
features of obesity (140). Overall, ginger consumption has the
potential in managing obesity; however, additional studies are
necessary to conrm these ndings.
Neuroprotective effect.—In vitro studies found that ginger
extract inhibited the expression of a wide range of inammation-
related genes in microglial-like cells (nonneuronal brain
cells) and protected brain cells from Abeta insult (too much
Abeta protein in the brain is linked to the development of
AD), suggesting that ginger may have neuroprotective effects
(141, 142). More research on the proposed health benets of
ginger in this area is warranted.
Black Pepper
Bioactive components.—Black pepper contains from 5 to 9%
piperine, the major active constituent. Black pepper also contains
alkamides, piptigrine, wisanine, and dipiperamide (143).
Bioactive components.—Ginger contains the following
nonvolatile pungent components: gingerols, shogaols, paradols,
and zingerone.
Nausea and vomiting.—Clinical trials show ginger (1 g/day)
may be safe and effective for decreasing nausea and vomiting
during pregnancy (102–105) or when induced by chemotherapy
(106). Furthermore, 500 mg oral ginger 1 h before surgery in
women who were undergoing laparoscopic cholecystectomy
is effective in decreasing the severity of postoperative nausea
and vomiting (107). In a double-blinded study, 500 mg ginger
2 times per day was effective in ameliorating antiretroviral-
induced nausea and vomiting (108). However, ginger with
prescription drugs may not reduce chemotherapy-induced
nausea as evidenced by a randomized, double-blind, placebo-
controlled trial in 162 patients (109).
Antioxidant and anti-inammatory effects.—Ginger and its
extracts, such as 6-gingerols and 6-shogaol, exhibited substantial
free-radical scavenging activities and inhibited production
of inammatory mediators [e.g., NO and Prostaglandin E2].
They also suppressed proinammatory transcription factor
(NF-κB) and activity of inammatory cytokines [e.g., tumor
necrosis factor–α (TNF-α)] and inhibited COX-2 (an enzyme
responsible for biochemical pathways activated in chronic
inammation) during in vitro studies (110–114). 6-Shogaol was
found to have much stronger inhibitory effects on arachidonic
acid release and NO synthesis than 6-gingerol (112–114). In a
recent human clinical trial, participants with osteoarthritis (OA)
received capsules containing 500 mg of ginger powder for
3 months, and their serum levels of TNF-α and interleukin-1β
(IL-1β) were decreased (115). Ginger also signicantly lowered
COX-1 protein expression in participants at increased risk for
early event in colorectal cancer (116).
Cardiovascular health.—Ginger has been reported to have
anti-inammatory, antioxidant, antiplatelet, antihypertensive,
and hypolipidemic effects (117–121). Although the relatively
few human trials involving ginger generally used low
doses yielding inconclusive results, dosages of 5 g or more
demonstrated signicant antiplatelet (anticlotting) activity
(117, 121). Early human studies suggested that up to 2 g dried
ginger is unlikely to cause platelet dysfunction when used
therapeutically (122). However, there is a synergistic effect on
antiplatelet aggregation when 1 g ginger per day was combined
with nifedipine (a BP-lowering drug; 123). A double-blind,
placebo-controlled trial with 85 hyperlipidimic subjects showed
3 g/day ginger for 45 days markedly lowered blood levels of
triglyceride, cholesterol, and LDL, with increased HDL, when
compared with a placebo control (120). In addition, a study with
rats indicated that ginger may prevent fat storage and reduce
body weight (124). More clinical trials are necessary before
denitive conclusions can be made about the cardiovascular
effects of ginger in humans.
Joint and muscle health.—Animal studies suggest that
ginger can reduce joint swelling, cartilage destruction, and
serum levels of inammatory cytokines associated with
rheumatoid arthritis and joint and muscle pain (125, 126). In a
randomized human trial, 11 days of oral administration of 2 g
raw or heat-treated ginger prior to exercise reduced muscle pain
induced by eccentric exercise and slightly reduced markers of
inammation and muscle function (127). It was also reported
that 4 g ginger supplementation can accelerate muscle strength
400 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
that BPB appears to have the potential to modulate perceived
appetite by lowering ‘hunger,’ ‘desire to eat,’ and ‘prospective
consumption’ and increasing ‘satiety’ and ‘fullness’ without
affecting gastrointestinal wellbeing. Further experiments are
needed to establish the relevant dose and mode of intake to
optimize the effects.
Enhancing nutrient bioavailability.—Piperine has a passive
diffusion mechanism, high apparent permeability coefcient,
and short clearance time (165). It was suggested that piperine
promtes its efcient permeation through the epithelial barrier in
the intestine (166). Piperine enhances the absorption of various
nutrients and drugs and functions as a bioavailability enhancer
of various substances such as coenzyme Q10, curcumin, and
tea polyphenols (145). For example, when curcumin was
administrated with piperine at 20 mg/kg, its bioavailability
increased by 154% in an animal study (167). Bioavailability
enhancing of curcumin could be a preventive effect of piperine
on the intestinal and hepatic metabolism of curcumin (168).
Studies have shown that piperine remarkably increased the
in vivo bioavailability of resveratrol by inhibiting its metabolism
and decreasing the required dose of resveratrol in a clinical
setting (169).
Mood and cognitive function.—Black pepper may exhibit
antidepressant-like activity and have a cognition-enhancing
effect via the regulation of neurotransmitter metabolism in
animals (170, 171).
Bioactive components.—The major active constituents of
turmeric are curcuminoids including curcumin (diferuloyl-
methane), demethoxycurcumin, bisdemethoxycurcumin, and
tetrahydrocurcumin. Curcumin is the active compound most
commonly studied using in vitro and in vivo (animal and human)
Antioxidative and anti-inammatory effects.—Curcumin
preparations in vitro have scavenged free radicals, inhibited
lipid peroxidation and LDL, oxidation, and prevented
deoxyribonucleic acid (DNA) oxidative damage. Turmeric
also has exhibited powerful anti-inammatory activity,
possibly by inhibiting COX-2, prostaglandins, leukotrienes,
and other inammatory mediators such as TNF-α, and NF-κB
(2, 3). In a randomized controlled trial (172), it was shown that
curcumin supplementation (daily dose of 1 g/day) over 8 weeks
signicantly decreased serum concentrations of proinammatory
cytokines in 59 subjects with a metabolic syndrome. There
were signicant reductions in serum concentrations of TNF-α,
IL-6, TGF-β, and MCP-1 following curcumin supplementation
(P < 0.001).
Cardiovascular health.—A number of laboratory, animal,
and human studies suggest that curcumin may have protective
effects on cardiac function, vascular health, and lipid proles
(173, 174). In an uncontrolled study, 10 healthy human
volunteers who received a dose of 500 mg curcumin per day
for 7 days had a 12% decrease in total serum cholesterol
levels and a 29% increase in HDL-C levels (175). Curcumin
also reduced cholesterol levels in acute coronary syndrome
patients in a clinical trial in which curcumin was administered
in various doses (45, 90, or 180 mg/day). It appeared that lower
doses of curcumin were more effective than higher doses in this
regard, in which 45 mg/day of curcumin reduced LDL and total
Antioxidant effect.—Piperine, the active compound of black
pepper, has been demonstrated within in vitro studies to protect
against oxidative damage by inhibiting or quenching free
radicals and reactive oxygen species. Both the oil and oleoresins
showed strong antioxidant activity in comparison with butylated
hydroxyanisole and butylated hydroxytoluene (143–145). Black
pepper or piperine treatment has also been evidenced to lower
lipid peroxidation in vivo and benecially inuence cellular
antioxidant status in a number of experimental situations of
oxidative stress (146, 147).
Anti-inammatory effect.—Piperine has revealed remarkable
anti-inammatory and analgesic activities (148). The anti-
inammatory activity of piperine has been conrmed in
many rat models (149). Both in vitro and in vivo rat models
found that piperine inhibited 5-lipoxygenase and COX-2, two
key enzymes involved in biosynthesis of proinammatory
mediators that cause inammation, pain and fever (150–152).
Piperine also reduced the levels of proinammatory cytokines
such as IL-1β, IL-6, and TNF-α levels and inhibited activation
of NF-κB within in vitro and in vivo animal studies (152–154).
In addition, piperine relieved pain in an arthritis animal model
(152, 155). Curcumin and piperine supplementation before and
after exercise can attenuate some aspects of muscle damage (156).
Antiallergic effect.—An animal model found that piperine
inhibited both histamine release and eosinophil inltration
and also suppressed allergic airway inammation and airway
hyperresponsiveness (157). Asthma is an inammatory disease
caused by irregular immune responses in the airway mucosa.
Piperine has shown deep inhibitory effects on airway inammation
in a murine model of asthma from supressing type 2 helper T cells
(Th2) cytokines (IL-4, IL-5, and IL-13), immunoglobulin E,
eosinophil CCR3 expression, and by enhanced transforming
growth factor–β (TGF-β) gene expression in the lungs.
Therefore, it can be considered as a possible immunomodulator
by downregulating Th2 cytokines (157).
Digestion aid.—Black pepper may accelerate the overall
digestive process by enhancing the activity of digestive
enzymes, increasing gastric acid and bile acid secretion, and
reducing food transit time (145). In animal studies, piperine was
found to enhance the activities of pancreatic amylase, lipase,
and chymotrypsin by 87, 37, and 30%, respectively, when
consumed through the diet (158).
Cardiovascular health.—Piperine has been shown to inhibit
lipid droplet accumulation in mouse macrophages that are
converted to foam cells in an animal study, suggesting it may
help retard the progression in which fatty deposits build up in
the arterial wall (159). Piperine also reduced plasma lipid and
lipoprotein levels in rats (160), inhibited platelet-derived growth
factor-BB-induced proliferation and migration of vascular
smooth muscle cells in blood vessels (161), and lowered blood
pressure in animals (162). More research is necessary to verify
the cardiovascular benets of black pepper.
Weight management.—Piperine may enhance energy
expenditure or thermogenesis through the sympathetic nervous
system by increasing levels of catecholamine and activating
the adrenal sympathetic nerves in animal studies (163). Zanzer
et al. (164) recently examined the postprandial effect of a
black pepper–based beverage (BPB) on glycaemia, appetite,
gastrointestinal well-being, gut hormones (peptide tyrosine–
tyrosine and GLP-1), and thyroid hormones postprandially after
a white wheat bread challenge in healthy adults, and concluded
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 401
a population of community-dwelling older adults. A signicant
time × treatment group interaction was observed for the
Montreal Cognitive Assessment (repeated-measures analysis;
time × treatment; F = 3.85, P < 0.05) in subjects who ingested
1500 mg/day Biocurcumax for 12 months. Subsequent analysis
revealed that this association was driven by a decline in function
of the placebo group at 6 months that was not observed in the
curcumin treatment group. In addition, curcumin may have
antidepressant effect. Chronic supplementation with curcumin
(1000 mg/day) produced a signicant antidepressant behavioral
response in depressed patients by a reduction of 17 item
Hamilton Depression Rating Scale and Montgomery-Asberg
Depression Rating Scale scores (195). Furthermore, curcumin
decreases inammatory cytokines IL-1β and TNF-α levela,
increases plasma brain-derived neurotrophic factor levels, and
decreases salivary cortisol concentrations
Joint and muscle health.—The anti-inammatory activity
properties of curcumin may also help this bioactive compound
maintain healthy joint function (196). In a well-described
animal model of rheumatoid arthritis, the arthritic index, a
clinical measure of joint swelling, was used as the primary
end point for assessing the effect of turmeric extracts on
joint inammation. The study showed turmeric extract
containing 41% curcuminoids was effective in preventing joint
inammation in rats (197). A number of human clinical trials
have demonstrated that curcumin acts as an analgesic and anti-
inammatory agent for the management of arthritis (198, 199).
Kuptniratsaikul et al. (200) found that patients with primary
knee OA who consumed a dose of 2 g/day turmeric extract for
6 weeks had similar pain relief as the patients who consumed
800 mg/day of ibuprofen (200). Haroyan et al. (201) compared
the effects of CuraMed® (Terry Naturally) 500 mg capsules
(333 mg curcuminoids) and Curamin® (Terry Naturally) 500 mg
capsules (350 mg curcuminoids and 150 mg boswellic acid)
taken orally 3 times a day for 12 weeks in 201 patients with OA
in a three-arm, randomized, double-blinded, placebo-controlled
trial. They found that curcumin complex reduced pain-related
symptoms in patients with OA, and curcumin in combination
with boswellic acid is more effective, presumably because of the
synergistic effects of curcumin and boswellic acid.
Blood glucose control.—In vitro and in vivo animal studies
have found that curcumin lowered blood glucose levels
through the suppression of glucose in the liver (202), reversed
insulin resistance in fat cell cultures (203), increased glucose
uptake into skeletal muscle (204), and stimulated pancreatic
beta-cell function (205). Turmeric supplementation has
been shown to improve glucose indexes. A randomized
clinical trial, in which patients with T2DM were given
two 300 mg doses of curcuminoids daily for 8 weeks,
found that curcumin had a favorable effect on endothelial
dysfunction in association with reductions of inammation
and oxidative stress in a similar manner to those randomized
to the prescription medication group (atorvastatin; 206). In a
recent clinical trial, 46 patients with NAFLD were given 3 g
turmeric in capsules each day for 12 weeks, and it was found
that turmeric consumption decreased serum levels of glucose,
insulin, and HOMA-IR (207).
Weight management.—In cell cultures and an animal model
for obesity, curcumin inhibited the formation of new blood
vessels (angiogenesis), decreased the transformation of young
fat cells into mature fat cells (adipogenesis), and reduced the
cholesterol levels with increased HDL concentrations (176).
In a 12 week randomized, double-blind, placebo-controlled trial
(177), subjects with T2D (n = 118), curcuminoid (1000 mg/day
plus piperine 10 mg/day) supplementation revealed signicant
reductions in serum levels of total cholesterol, non–HDL-C
and lipoprotein(a) with elevations in serum HDL-C levels in
the curcuminoids group as compared with the placebo group.
Thus, curcuminoids supplementation could contribute to a
reduced risk of cardiovascular events in dyslipidemic patients
with T2D. Moreover, 12 weeks of curcumin (2000 mg/day
Longvida®; Verdure Sciences) supplementation improved
resistance of arterial endothelial function by increasing vascular
NO bioavailability and reducing oxidative stress, while also
improving conduit artery endothelial function in healthy middle-
aged and older adults (178). In addition, curcumin can improve
metabolic proles in patients with metabolic syndrome (179).
Gastrointestinal health.—A pilot trial examined the effect of
standardized turmeric extract on symptoms of irritable bowel
syndrome (a functional bowel disorder) in 207 otherwise
healthy adults. Administrating a dose of either 72 or 144 mg
turmeric extract for 8 weeks reduced the pain/discomfort score
signicantly (22–25%), and approximately two-thirds of the
subjects reported an improvement in symptoms after treatment
(180). A randomized, double-blind trial in patients with ulcerative
colitis suggested that consumption of 2 g/day curcumin reduced
recurrence rates and improved the clinical activity index (181).
In addition, in vitro and in vivo animal studies suggested that
curcumin has anti-H. pylori activity and eradicated H. pylori
from infected mice (182, 183). In a recent randomized trial
(184), it was shown that an addition of curcumin (500 mg/day)
on top of the standard antihelicobacter regimen in patients with
peptic ulcers is safe and improves dyspepsia symptoms but has
no enhancing effect on the eradication of H. pylori infection.
Curcumin has been shown to be effective against development
of hepatic steatosis and its progression to steatohepatitis (185,
186). In a randomized trial, an 8 week supplementation of
curcumin was associated with a signicant reduction in liver
fat content (78.9% improvement in the curcumin versus 27.5%
improvement in the placebo group) in patients with nonalcoholic
fatty liver disease (NAFLD; 186). There were also signicant
reductions in BMI and serum levels of total cholesterol, LDL-C,
triglycerides, liver enzymes, and uric acid when compared with
the placebo group (185, 186).
Brain health and cognitive function.—Preventing the
accumulation of Abeta aggregation is an important factor
in maintaining healthy brain function. The accumulation of
Abeta occurring in the brain is one of the leading causes of
neurodegeneration (187). Curcumin enhanced Abeta clearance
and reduced Abeta and plaque burdens in animal studies (188, 189).
Animal studies with curcumin also found that this bioactive
ingredient has improved memory retention and prevented
oxidative damage (190, 191). In addition, a mouse study
showed that curcumin protected against the development of brain
blood vessel spasm and limited secondary brain tissue death
as a result of an inadequate blood supply (192). A population-
based cohort study in Singapore involving over 1000 mentally
competent Asian subjects aged 60–93 years showed that regular
turmeric consumption helped preserve cognitive function even
when low-to-moderate curry levels were consumed (193).
More recently, Rainey-Smith et al. (194) investigated the
ability of a curcumin formulation to prevent cognitive decline in
402 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
extract also plays a role in its ability to moderate the metabolism
of glucose in the digestive tract (220). Specically, a soluble ber
in fenugreek, galactomannan, becomes viscous and thickens the
intestinal contents, helping to maintain healthy glucose absorption
(221). In a human study, when fenugreek was incorporated into
food, it reduced the glycemic index (GI) by 21% compared with
standard food not treated with fenugreek (222). Furthermore, a
recent randomized, controlled crossover trial in healthy human
subjects documented that replacing 10% of rened wheat our
with fenugreek seed powder signicantly reduced the glycemic
response and the GI of buns and atbreads (223). It has been also
reported that fenugreek seeds at 10 g/day signicantly decreased
fasting blood glucose and HbA1c, serum levels of insulin,
homeostatic model assessment for insulin resistance, and total
cholesterol and triglycerides, and it increased serum levels of
adiponectin in type 2 diabetic patients (224).
Satiety and weight management.—Because of its high ber
content, fenugreek could help promote satiety, which may
potentially support weight management. Hydroxyisoleucine, a
fenugreek extract, reduced body weight in obese mice (225).
In a single-blind, randomized, crossover study, 8 g fenugreek
ber in a breakfast meal increased feelings of fullness and
reduced hunger, as well as reduced energy intake at lunch in
18 healthy obese subjects (226). Another small-scale, double-
blind, randomized, placebo-controlled human trial showed
a consumption of 1200 mg fenugreek seed extract daily for
14 days signicantly decreased fat consumption by 17%
compared with a placebo in 12 healthy subjects (227).
Exercise and physical performance.—Prolonged exercise
depletes muscle reserves of glycogen, which can place
limitations on physical performance. The speed of glycogen
resynthesis in muscle can, therefore, determine the rate of
recovery after exercise. A recent study in trained male cyclists
documented that those who ingested a glucose beverage
with fenugreek extract (containing 2 mg/kg body weight of
4-hydroxyisoleucine) right after high-intensity exercise had a
63% greater rate of muscle glycogen resynthesis than those
who consumed the glucose beverage without the fenugreek
extract (228). However, in a subsequent study by the same
research group using a low-intensity exercise protocol, the
fenugreek extract had no effects on glycogen resynthesis
(229). Nevertheless, an animal study suggested fenugreek
extract may have benecial effects on endurance capacity
by increasing fatty acid use and sparing glycogen. An animal
study found that mice that received a fenugreek extract
(300 mg/kg) had increased exercise endurance compared with
those who did not (230).
Liver health.—Animal studies suggest fenugreek may
help protect against liver changes induced by chronic alcohol
consumption. Administration of fenugreek seed extract to
alcohol-fed rats (200 mg/kg) reduced the levels of lipid
peroxidation products and protein carbonyl content, increased
the activities of antioxidant enzymes, and restored the levels
of thiol groups compared with the control (231). Animal
experiments have also found that fenugreek reduced the
triglyceride accumulation in the liver (232), a hallmark feature
of hepatic steatosis, and regressed cholesterol gallstones
formation (233); both effects were accompanied by signicant
reductions in blood lipid levels.
Sexual health.—Fenugreek seed extract has demonstrated
hormone modulatory activity, providing biological plausibility
buildup of fat in the mature cells, which has implications for
lowering body fat and body weight gain in mice. Therefore,
curcumin may have a potential benet in weight control. In a
human study on 40 subjects who had a weight loss <2% after
30 days of diet and intervention lifestyle, curcumin
administration for an additional 30 days increased weight loss
from 1.88 to 4.91%, enhanced body fat reduction percentage
from 0.70 to 8.43%, and enhanced BMI reduction from 2.10
to 6.43% (208). Supplementation with curcumin (phytosomal
form; 1000 mg/day) was associated with a reduction in BMI and
waist circumference in patients diagnosed with NAFLD (209).
Chemoprevention.—Curcumin inhibited the proliferation of
various tumor cells in culture, prevented carcinogen-induced
cancers in rodents, and inhibited the growth of human tumors
in various models (210). Numerous mechanisms for these
outcomes have been implicated, and human data in this area
are limited to a small number of study subjects. Large doses
of oral curcumin have biological activity in some patients with
pancreatic cancer and marked tumor regression (73%) was
observed in one subject (211).
Bioactive components.—The chemical components
of fenugreek seeds include a large carbohydrate fraction
(mucilaginous ber, galactomannan), steroidal saponins
(e.g., diosgenin and trigogenin), free amino acids (e.g.,
hydroxyisoleucine and lysine), avonoids. and alkaloids
(e.g., gentianine and trigonelline). Three important chemical
constituents with functionality are steroidal sapogenins
(converted from saponin while passing through human intestinal
tract), galactomannans, and 4-hydroxyisoleucine.
Lipid metabolism and vascular health.—Several animal and
human studies have identied signicant lipid-lowering activity
with different fenugreek preparations (212–217). An animal
study indicated that fenugreek fractions rich in steroid saponins
decreased total plasma cholesterol but did not change triglyceride
levels (212). The ber content of fenugreek extract helped
moderate the metabolism of lipids in the digestive tracts of rats
(213, 214). In a hamster model of diabetes, a fenugreek-active
compound (4-hydroxyisoleucine) decreased elevated plasma
triglyceride by 33% and total cholesterol levels by 22% (215).
Human data suggest that higher intakes may be required for
lipid-lowing activity to become signicant. An open label
clinical trial using a daily dose of 12.5–18 g seed powder in
healthy volunteers demonstrated signicant reductions in total
cholesterol and LDL-C levels (216). Another clinical trial study
also showed that serum levels of triglycerides and VLDL-C
were decreased signicantly (30 and 30.6%, respectively) after
taking 10 grams/day powdered fenugreek seeds soaked in hot
water for 8 weeks in type 2 diabetic patients (217). Further
well-controlled, double-blind research is warranted, especially
to determine the optimum dosage levels.
Blood glucose metabolism.—Animal and in vitro studies have
demonstrated that 4-hydroxyisoleucine, an amino acid extracted
from fenugreek seeds, is a key component in supporting
glucose and lipid metabolism (218). Administrating fenugreek
seed extract improved insulin signaling and sensitivity, which
promoted the cellular actions of insulin in fructose-fed animals.
This effect was comparable with that of metformin, a drug used
to treat high blood sugar (219). The ber content of fenugreek
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 403
evidence that rosemary may promote brain health by inhibiting
both acetylcholin esterase and butyrylcholinesterase in vitro,
which may help facilitate communication among cells in the
brain (249, 250). A protective effect on dopaminergic neural
cells (which involve behavior and cognition, mood, attention,
and learning) has been observed in a number of rosemary
constituents (251, 252). Furthermore, carnosic acid may
improve cell viability and blood ow to the brain, based on in
vitro experiments (251, 253).
Vascular health.—Evidence suggests that rosemary extract
could inhibit LDL-C oxidation in a biologically relevant human
cell culture system (254). Rosemary has shown antithrombotic
activity and may improve endothelial function both in vitro
and in vivo (255, 256). At a 5% concentration, rosemary
signicantly improved vascular function by inhibiting platelet
reactivity and arterial blood clot formation as well as enhancing
ow-mediated vasodilation in animals (256). Further, rosemary
extract inhibited rabbit lung angiotensin I–converting enzyme
(ACE) in vitro (257). This inhibition leads to less production
of a chemical that causes arteries to constrict, suggesting that
rosemary extract may have an antihypertensive effect. Clinical
studies are needed to determine whether this effect is signicant
in humans.
Blood glucose control.—In an animal model, a high dose of
rosemary extract (100 mg/kg or higher) signicantly lowered
blood glucose levels and increased serum insulin concentrations
in diabetic rabbits compared with 50 mg/kg (258). Rosemary
activated PPAR-γ, which plays an essential role in the regulation
of cellular functions and metabolism, leading to lower blood
levels of fatty acids and glucose (259). Furthermore, rosemary
is a potential inhibitor of alpha-glucosidase, which may help
reduce sugar absorption (260). Rosemary may also inhibit AGE
formation in vitro (261), which suggests it has the potential
to protect against the development of diabetic complications.
However, more studies are required in animals and humans to
conrm this hypothesis.
Skin care.—Destruction of collagen is a hallmark of skin
aging as a result of exposure to UV irradiation in which the
matrix metalloproteinases (MMPs) play important roles
in destructive processes. A water-soluble extract inhibited
UV-induced MMP-1 and showed potential benets for
preventing skin photodamage in vitro (262). Further, carnosic
acid has demonstrated photoprotective action on human skin
cells exposed to UVA light in vitro. Rosemary extract inhibited
oxidative damage to skin-surface lipids in both in vitro and in
vivo studies (263). Rosemary may be a good candidate for an
antiskin aging agent, but more human data are needed.
Heptoprotective effects.—Rosemary extract has reduced
toxic chemical-induced liver damage and cirrhosis and has
improved detoxication systems in an animal model (264).
Consumption of 200 mg/kg leaf extract can limit weight gain
induced by a high-fat diet and protect against obesity-related
liver steatosis (build up of fat in the liver) in mice. However,
administrating a lower dose of the leaf extract at 20 mg/kg body
weight was ineffective for this purpose (265).
Chemopreventive and anticarcinogenic potential.—In vitro
studies suggest that rosemary extract may reduce the effects of
carcinogenic or toxic agents in many human cell lines (266).
One mechanism through which constituents in rosemary may
exert anticancer effects is by reducing the expression of a
number of proinammatory genes (267).
for relieving menopausal symptoms. In a randomized, placebo-
controlled trial, treatment with fenugreek dehusked seed
extract at 600 mg/day resulted in a signicant reduction
in menopausal symptoms; women aged 40–65 years in the
treatment group reported signicantly less daytime hot
ashes and night sweats at 12 weeks (234). In addition to
improvements on various postmenopausal discomforts and
quality of life of women, there was a signicant increase
in plasma estradiol in the extract-treated group (235).
Moreover, Rao et al. (236) reported that fenugreek extract
supplementation resulted in a signicant increase in blood-
free testosterone and E2 levels as well as sexual desire and
arousal, compared with the placebo. The results indicate that
fenugreek extract may be a useful treatment for increasing
sexual arousal and desire in women.
Recently, clinical studies also documented the effect of
a specialized fenugreek seed extract (e.g., Testofen) on the
symptoms of possible androgen deciency, sexual function,
and serum androgen concentrations in healthy aging males
(237–240). Supplementation of the extract at a dose of
600 mg/day for 12 weeks improved the Aging Male Symptom
questionnaire, a measure of possible androgen deciency
symptoms; sexual function; and increased both total serum
testosterone and free testosterone in healthy middle-aged
and older men (237). Testofen demonstrated a signicant
positive effect on physiological aspects of libido and may
assist to maintain normal healthy testosterone levels (239).
A protodioscin-enriched fenugreek seed extract (500 mg/day)
increased serum-free testosterone levels up to 46% as well as
sperm counts, and it improved mental alertness, mood, and
libido in the male study population (238).
Bioactive components.—Rosemary contains phenolic acids
and diterpenes including carnosic acid, carnosol, caffeic acid
and its derivatives (i.e., rosmarinic acid), avonoids (apigenin,
diosmin, luteolin), and tannins. Rosemary also contains volatile
oils that consist of cineole, pinene, and camphor.
Antioxidant and anti-inammatory effects.—Numerous
laboratory tests indicate that rosemary has strong antioxidant
properties. Carnosic acid and carnosol likely account for
over 90% of its antioxidant activity (241). Carnosic acid and
carnosol reduced membrane damage by 40–50% and inhibited
lipid peroxidation by 88–100 and 38–89%, respectively,
under oxidative stress conditions in a cell culture testing.
Both compounds also lowered DNA damage induced by a
dietary oxidant (242). Rosemary extract enhanced antioxidant
defenses and improved antioxidant status in aged rats (243).
Rosemary suppressed the activation of inammatory
cytokines such as NF-κB and IL-1β and shut down specic
enzymes (COX-2) involved in inammation during in vitro
experiments (244, 245).
Cognition, mental health, and neuroprotection.—
Inhalation of rosemary and lavender oils enhanced cognitive
function in a randomized study of 140 subjects using a
cognitive assessment battery test and self-assessment mood
scale (246). The aroma of rosemary oil reduced test-taking
stress in graduate students (247). Rosemary extract had an
antidepressant-like effect through an interaction with the
monoaminergic system in a rat study (248). There is emerging
404 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
well documented (290, 291). Garlic stimulates the synthesis of
NO (292, 293) and inhibits ACE activity (294). Furthermore,
garlic-derived organic polysuldes are converted by red blood
cells into hydrogen sulde gas, which leads to vasorelaxation
via vascular smooth-muscle cell signaling pathway (295).
This study demonstrated a new mechanism responsible for
garlic-mediated attenuation of hypertension. A meta-analysis
indicated that garlic reduced SBP by 16.3 mmHg and DBP by
9.3 mmHg in patients with an elevated SBP (296). A recent
review documented that garlic supplementation reduced
SBP by 7–16 mmHg and 5–9 mmHg for DBP based on four
meta-analyses and two original studies (289).
Antithrombotic and anticoagulant properties.—
Antithrombotic activity has been documented for garlic extract
in both in vitro and in vivo human studies (297–299). Garlic
has been shown to inhibit platelet aggregation (stickiness)
by inhibiting COX-1 activity and thromboxane A2 formation
(a clotting factor) during in vitro studies using human platelets
(297, 299). Additionally, garlic extracts have thr potential to
activate brinolytic activity, increasing brinolysis (dissolving
small blood clots; 300, 301). In a placebo-controlled study that
involved 30 patients with coronary artery disease, administration
of garlic extract (at the dose equivalent to 4 g garlic) increased
markedly brinolytic activity (299). However, it seems that
raw garlic or garlic oil does not impair platelet function or alter
vasoreactivity and brinolytic potential in healthy volunteers
Hypoglycemic activity.—Garlic has blood glucose–lowering
properties in diabetic rats (305–307). When the rats were treated
with a high dose (500 versus 50 mg/kg) of raw garlic, blood
glucose, cholesterol, and triglyceride levels were markedly
affected (308). Both garlic oil and diallyl trisulde improved
glycemic control in diabetic rats through increased insulin
secretion and increased insulin sensitivity (309). In a human
trial, it was demonstrated that treatment with time-released garlic
product (Allicor) resulted in better metabolic control because
of the lowering of fasting blood glucose and triglyceride levels
(310). More recently, Wang et al. (311) systematically evaluated
the clinical efcacy and safety of garlic supplement in the
management of T2DM and found a signicant reduction in the
level of fasting blood glucose in from 1 to 2 weeks to 24 weeks,
as well as signicantly decrease in fructosamine and glycated
hemoglobin (both in 12 and 24 weeks) were achieved in the
garlic group. Thus, current data conrm that garlic supplements
play a positive and sustained role in blood glucose and favorable
lipoprotein regulation in the management of T2DM.
Brain health.—Experimental evidence has shown that some
garlic-derived products have a protective effect against ischemic
brain injury, thereby improving learning and memory retention
(312–314). In vitro and animal studies also suggest garlic could
protect neurons from Abeta-induced neurotoxicity and apoptosis
(315–317). These preclinical studies suggest that garlic helps
prevent cognitive decline associated with AD (314–317).
However, observation in humans is not available yet.
Immunomodulatory activity.—In vitro and in vivo (animal)
studies have found that garlic and its constituents have several
immune-enhancing effects such as stimulation of lymphocyte
proliferation and interferon-γ release and enhancement of
macrophage phagocytosis and killer cell activity (318–321).
However, more studies are needed to understand the signicance
of these emerging data.
Bioactive components.—Many of the biological effects of
garlic are attributed to the allicin, ajoene, and other organosulfur
constituents such as S-allyl-L-cysteine (SAC). Alliin, which
is found predominantly in garlic, is cleaved by alliinase
to form allicin when garlic is crushed or chopped. Allicin,
which is unstable in an aqueous solution, rapidly decomposes
nonenzymatically to other sulfur-containing compounds
including allylpropyl disulde, diallyl sulde, diallyl disulde,
diallyl trisulde, diallyl tetrasuldes, ajoene, and vinyldithiines.
SAC is formed from γ-glutamylcysteines during long-term
incubation of crushed garlic in aqueous solutions and is
the primary organosulfur constituent in aged garlic extract.
In addition, phytoalexin (e.g., allixin) is found to have certain
biological activity. Allicin has been found to be the compound
most responsible for the “hot” sensation of raw garlic.
Anti-inammatory activity.—Garlic and its sulfur-containing
compounds exert anti-inammatory properties through the
inhibition of NF-κB activation (a transcription factor that
regulates inammatory response genes), iNOS, and COX-2
expression during in vitro and animal studies (268–270). In a
clinical trial, daily dose supplementation of a 1000 mg garlic
tablet for 12 weeks signicantly improved stiffness, pain, and
physical function in overweight or obese women with OA (271).
Cardiovascular health and endothelial function.—Garlic has
traditionally been used to promote cardiovascular health through
a variety of mechanisms (268, 272–274). Evidence from in vitro,
animal, and human research has shown that taking garlic may
slow the development of atherosclerotic process (hardening of
the arteries; 275, 276), a condition that can lead to heart attacks
and strokes, by benecially reducing fatty streak formation
in blood vessels and atherosclerotic plaque size (277, 278),
inhibiting oxidation of LDL-C (as oxidized LDL is what
damages the blood vessels; 279, 280), suppressing inammatory
cell adhesion to endothelial cells (280), and improving impaired
endothelial function (276, 281, 282). Some human trials
showed that garlic slowed the development of atherosclerosis
as measured by ultrasound (283) or increased brachial artery ow-
mediated, endothelium-dependent dilation by 44% (284). More
recently, Szulinska et al. (285) demonstrated that supplementation
with 400 mg of garlic extract favorably modied endothelial
biomarkers (e.g., CRP, and plasminogen activator inhibitor–1,
and LDL-C) associated with cardiovascular risk. Furthermore,
supplementation of garlic powder tablet (1200 μg allicin/tab) twice
daily could prevent carotid intima-media thickness progression in
patients with coronary artery disease (286).
Blood cholesterol–lowering effects.—There is contradictory
evidence about the effects of garlic on cholesterol and
triglyceride levels. Animal and human cell lines studies have
demonstrated that garlic may reduce blood lipids levels via
inhibition of HMG-CoA reductase (similar to the mechanism
by which statins work) or other key enzymes involved in
cholesterol and fatty acid synthesis (287). A meta-analysis
found garlic reduced blood total cholesterol (7.3 mg/dL) and
triglycerides (9.7 mg/dL) but exhibited no signicant effect
on LDL or HDL (288). A later review documented that garlic
supplementation reduced total cholesterol by 7.4–29.8 mg/dL
in eight meta-analyses (289).
Blood pressure–lowering effects.—The antihypertensive
effects of garlic and its constituents in vitro and in vivo are
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 405
(25) Saito, M., & Yoneshiro, T. (2013) Curr. Opin. Lipidol. 24,
71–77. doi:10.1097/MOL.0b013e32835a4f40
(26) Srinivasan, K. (2013) Food Funct. 4, 503–521. doi:10.1039/
(27) Lee, C.Y., Kim, M., Yoon, S.W., & Lee, C.H. (2003) Phytother.
Res. 17, 454–458. doi:10.1002/ptr.1172
(28) Manjunatha, H., & Srinivasan, K. (2007) Can J. Physiol
Pharmacol. 85(6):588-96
(29) Raghavendra, R.H., & Naidu, K.A. (2009) Prostaglandins,
Leukotrienes Essent. Fatty Acids 81, 73–78. doi:10.1016/j.
(30) Guarini, G., Ohanyan, V.A., Kmetz, J.G., DelloStritto, D.J.,
Toppil, R.J., Thodeti, C.K., Meszaros, J.G., Dmron, D.S., &
Bratz, I.N. (2012) Am. J. Physiol. Heart Circ. Physiol. 303,
H216–H223. doi:10.1152/ajpheart.00011.2012
(31) Ahuja, K.D., & Ball, M.J. (2006) Br. J. Nutr. 96, 239–242.
(32) Ahuja, K.D., Robertson, I.K., Geraghty, D.P., &
Ball, M.P. (2007) Eur J. Clin Nutr. 61, 326–333. doi:10.1038/
(33) Yuan, L.J., Qin, Y., Wang, L., Zeng, Y., Chang, H., Wang, J.,
Wang, B., Wan, J., Chen, S.H., Zhang, Q.Y., Zhu, J.D.,
Zhou, Y., & Mi, M.T. (2016) Clin. Nutr. 35, 388–393.
(34) Chaiyata, P., Puttadechakum, S., & Komindr, S. (2003) J. Med.
Assoc. Thai. 86, 854–860
(35) Ahuja, K.D., Robertson, I.K., Geraghty, D.P., &
Ball, M.J. (2006) Am. J. Clin. Nutr. 84, 63–69. doi:10.1093/
(36) Chaiyasit, K., Khovidhunkit, W., & Wittayalertpanya, S. (2009)
J. Med. Assoc. Thai. 92, 108–113
(37) Islam, M.S., & Choi, H. (2008) Phytother. Res. 22(8):1025–1029.
(38) Kwon, D.Y., Hong, S.M., Ahn, I.S., Kim, Y.S., Shin, D.W., &
Park, S. (2009) Nutrition 25, 790–799. doi:10.1016/j.
(39) Rau, O., Wurglics, M., Dingermann, T., Abdel-Tawab, M.,
Schubert-Zsilavecz, M. (2006) Pharmazie 61, 952–956
(40) Zsombok, A. (2013) J. Diabetes Complications 27, 287–292.
(41) Yoshioka, M., St-Pierre, S., Suzuki, M., & Tremblay, A. (1998)
Br. J. Nutr. 80, 503–510. doi:10.1017/S0007114598001597
(42) Westerterp-Plantenga, M.S., Smeets, A., & Lejeune, M.P. (2005)
Int. J. Obes. (Lond.) 29, 682–688. doi:10.1038/sj.ijo.0802862
(43) Janssens, P.L., Hursel, R., & Westerterp-Plantenga, M.S. (2014)
Appetite 77, 44–49. doi:10.1016/j.appet.2014.02.018
(44) Zhang, L.L., Liu, D.Y., Ma, L.Q., Luo, Z.D., Cao, T.B., Zhong, J.,
Yan, Z.C., Wang, L.J., Zhao, Z.G., Zhu, S.J., Schrader, M.,
Thilo, F., Zhu, Z.M., & Tepel, M. (2007) Circ. Res. 100,
1063–1070. doi:10.1161/01.RES.0000262653.84850.8b
(45) Diepvens, K., Westerterp, K.R., & Westerterp-Plantenga, M.S.
(2007) Am. J. Physiol. Regul. Integr. Comp. Physiol. 292,
R77–R85. doi:10.1152/ajpregu.00832.2005
(46) Lejeune, M.P., Kovacs, E.M., & Westerterp-Plantenga, M.S.
(2003) Br. J. Nutr. 90, 651–659. doi:10.1079/BJN2003938
(47) Hachiya, S., Kawabata, F., Ohnuki, K., Inoue, N., Yoneda, H.,
Yazawa, S., & Fushiki, T. (2007) Biosci. Biotechnol. Biochem.
71, 671–676. doi:10.1271/bbb.60359
(48) Kawabata, F., Inoue, N., Yazawa, S., Kawada, T., Inoue, K., &
Fushiki, T. (2006) Biosci. Biotechnol. Biochem. 70, 2824–2835.
(49) Snitker, S., Fujishima, Y., Shen, H., Ott, S., Pi-Sunyer, X.,
Furuhata, Y., Sato, H., & Takahashi, M. (2009) Am J. Clin. Nutr.
89, 45–50. doi:10.3945/ajcn.2008.26561
(50) Janssens, P.L., Hursel, R., Martens, E.A., & Westerterp-
Plantenga, M.S. (2013) PLoS One 8, e67786. doi:10.1371/
(1) Tapsell, L.C., Hemphill, I., Cobiac, L., Patch, C.S.,
Sullivan, D.R., French, M., Roodenrys, S., Keogh, J.B.,
Clifton, P.M., Williams, P.G., Fazio, V.A., & Inge, K.E. (2006)
Med. J. Aust. 185, S4–24
(2) Kaefer, C.M., & Milner, J.A. (2008) J. Nutr. Biochem. 19,
347–361. doi:10.1016/j.jnutbio.2007.11.003
(3) Iriti, M., Vitalini, S., Fico, G., & Faoro, F. (2010) Molecules 15,
3517–3555. doi:10.3390/molecules15053517
(4) Yashin, A., Yashin, Y., Xia, X., & Nemzer, B. (2017)
Antioxidants 6, 70. doi:10.3390/antiox6030070
(5) Srinivasan, K. (2005) Food Rev. Int. 21, 167–88. doi:10.1081/
(6) Barnes, P.M., Bloom, B., & Nahin, R.L. (2007) Complementary
and Alternative Medicine Use Among Adults and Children:
United States, 2007, National Health Statistics Reports; No. 12,
National Center for Health Statistics, Hyattsville, MD
(7) Clarke, T.C., Black, L.I., Stussman, B.J., Barnes, P.M., &
Nahin, R.L. (2015) Trends in the Use of Complementary Health
Approaches Among Adults: United States, 2002–2012, National
Health Statistics Reports; No. 79, National Center for Health
Statistics, Hyattsville, MD
(8) Su, D., & Li, L. (2011) J. Health Care Poor Underserved 22,
296–310. doi:10.1353/hpu.2011.0002
(9) Isbill, J., Kandiah, J., & Khubchandani, J. (2018) Health
Promot. Perspect. 8, 33–40. doi:10.15171/hpp.2018.04
(10) Opara, E.I., & Chohan, M. (2014) Int. J. Mol. Sci. 15,
19183–19202. doi:10.3390/ijms151019183
(11) Neveu, V., Perez-Jiménez, J., Vos, F., Crespy, V., du Chaffaut, L.
(2010) Database (Oxford) 2010, bap024. doi:10.1093/database/
(12) Craig, W.J. (1999) Am. J. Clin. Nutr. 70, 491–499. doi:10.1093/
(13) Tuohy, K.M., Conterno, L., Gasperotti, M., & Viola, R. (2012)
J. Agric. Food Chem. 61, 8776–8782. doi:10.1021/jf2053959
(14) Etxeberria, U., Fernndez-Quintela, A., Milagro, F.I., Aguirre, L.,
Martínez, J.A., & Portillo, M.P. (2013) J. Agric. Food Chem. 61,
9517–9533. doi:10.1021/jf402506c
(15) Lv, J., Qi, L., Yu, C., Yang, L., Guo, Y., Chen, Y., Bian, Z.,
Sun, D., Du, J., Ge, P., Tang, Z., Hou, W., Li, Y., Chen, J.,
Chen, Z., & Li, L. (2015) BMJ. 351, h3942. doi:10.1136/bmj.
(16) Chopan, M., & Littenberg, B. (2017) PLoS ONE 12, e0169876.
(17) Chen, Y.H., Zou, X.N., Zheng, T.Z., Zhou, Q., Qiu, H., Chen, Y.L.,
He, M., Du, J., Lei, H.K., & Zhao, P. (2017) Chin. Med. J.
(Engl.) 130, 2241–2250. doi:10.4103/0366-6999.213968
(18) Li, Q., Cui, Y., Jin, R., Lang, H., Yu, H., Sun, F., He, C.,
Ma, T., Li, Y., Zhou, X., Liu, D., Jia, H., Chen, X., &
Zhu, Z. (2017) Hypertension 70, 1291–1299. doi:10.1161/
(19) Anandakumar, P., Kamaraj, S., Jagan, S., Ramakrishnan, G.,
Vinodjkumar, R., & Devaki, T. (2008) Phytother. Res. 22,
529–533. doi:10.1002/ptr.2393
(20) Manjunatha, H., & Srinivasan, K. (2007) Can. J. Physiol.
Pharmacol. 85, 588–596. doi:10.1139/y07-044
(21) Spiller, F., Alves, M.K., Vieira, S.M., Carvalho, T.A.,
Leite, C.E., Lunardelli, A., Poloni, J.A., Cunha, F.Q., &
de Oliviera, J.R. (2008) J. Pharm. Pharmacol. 60, 473–478.
(22) Kang, J.H., Kim, C.S., Han, I.S., Kwanda, T., & Yu, R. (2007)
FEBS Lett. 581, 4389–4396. doi:10.1016/j.febslet.2007.07.082
(23) Nilius, B., & Appendino, G. (2013) Rev. Physiol. Biochem.
Pharmacol. 164, 1–76. doi:10.1007/112_2013_11
(24) Yang, S., Liu, L., Meng, L., & Hu, X. (2019) Chem.-Biol.
Interact. 297,1–7
406 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
(78) Mollazadeh, H., & Hosseinzadeh, H. (2016) Iran J. Basic Med.
Sci. 19, 1258–1270. doi:10.22038/ijbms.2016.7906
(79) Gupta, J.S., Puri, S., Misra, A., Gulati, S., & Mani, K. (2017)
Lipids Health Dis. 16, 113. doi:10.1186/s12944-017-0504-8
(80) Akilen, R., Pimlott, Z., Tsiami, A., & Robinson, N. (2013)
Nutrition 29, 1192–1196. doi:10.1016/j.nut.2013.03.007
(81) Costello, R.B., Dwyer, J.T., Saldanha, L., Bailey, R.L.,
Merkel, J., & Wambogo, E. (2016) J. Acad. Nutr. Diet 116,
1794–1802. doi:10.1016/j.jand.2016.07.015
(82) Medagama, A.B. (2015) Nutr. J. 14, 108. doi:10.1186/s12937-
(83) Allen, R.W., Schwartzman, E., Baker, W.L., Coleman, C.I., &
Phung, O.J. (2013) Ann. Fam. Med. 5, 452–459. doi:10.1370/afm.1517
(84) Qin, B., Polansky, M.M., & Sato, Y. (2009) J Nutr Biochem.
(85) Anderson, R.A. (2008) Proc. Nutr. Soc. 67, 48–53. doi:10.1017/
(86) Zhu, R., Liu, H., Liu, C., Wang, L., Ma, R., Chen, B., Li, L.,
Niu, J., Fu, M., Zhang, D., & Gao, S. (2017) Pharmacol. Res.
122, 78–89. doi:10.1016/j.phrs.2017.05.019
(87) Camacho, S., Michlig, S., de Senarclens-Bezençon, C.,
Meyalan, J., Pzzoli, M., Markram, H., & le Coutre, J. (2015)
Sci. Rep. 5, 7919. doi:10.1038/srep07919
(88) Mang, B., Wolters, M., Schmitt, B., Klb, K., Lichtighagen, R.,
Stichtenoth, D.O., & Hahn, A. (2006) Eur. J. Clin. Invest. 36,
340–344. doi:10.1111/j.1365-2362.2006.01629.x
(89) Hlebowicz, J., Darwiche, G., Björgell, O., & Almér, L.O. (2007)
Am. J. Clin. Nutr. 85, 1552–1556. doi:10.1093/ajcn/85.6.1552
(90) Solomon, T.P., & Blannin, A.K. (2007) Diabetes Obes. Metab.
9, 895–901. doi:10.1111/j.1463-1326.2006.00694.x
(91) Solomon, T.P., & Blannin, A.K. (2009) Eur. J. Appl. Physiol.
105, 969–976. doi:10.1007/s00421-009-0986-9
(92) Hlebowicz, J., Hlebowicz, A., Lindstedt, S., Björgell, O.,
Höglumd, P., Holst, J.J., Darwiche, G., & Almér, L.O. (2009)
Am. J. Clin. Nutr. 89, 815–821. doi:10.3945/ajcn.2008.26807
(93) Ziegenfuss, T.N., Hofheins, J.E., Mendel, R.W., Landis, J., &
Anderson, R.A. (2006) J. Int. Soc. Sports. Nutr. 3, 45–53.
(94) Altschuler, J.A., Casella, S.J., MacKenzie, T.A., & Curtis, K.M.
(2007) Diabetes Care 30, 813–816. doi:10.2337/dc06-1871
(95) Blevins, S.M., Leyva, M.J., Brown, J., Wrigh, J.,
Scoeld, R.H. & Aston, C.E. (2007) Diabetes Care. 30,
2236–2237. doi:10.2337/dc07-0098
(96) Suppapitiporn, S., Kanpaksi, N., & Suppapitiporn, S. (2006)
J. Med. Assoc. Thai. 89, S200–S205
(97) Vanschoonbeek, K., Thomassen, B.J., Senden, J.M.,
Wodzig, W.K.W.H., & van Loon, L.J.C. (2006) J. Nutr. 136,
977–980. doi:10.1093/jn/136.4.977
(98) Moselhy, S.S., & Ali, H.K. (2009) Biol. Res. 42, 93–98.
(99) Kanuri, G., Weber, S., Volynets, V., Spruss, A., Bischoff, S.C., &
Bergheim, I. (2009) J. Nutr. 139, 482–487. doi:10.3945/jn.108.100495
(100) Peterson, D.W., George, R.C., & Scaramozzino, F. (2009)
J Alzheimers Dis. 17, 585–597. doi:10.3233/JAD-2009-1083
(101) Kim, D.S., Kim, J.Y., & Han, Y.S. (2007) J. Altern.
Complement. Med. 13, 333–340. doi:10.1089/acm.2006.6107
(102) Keating, A., & Chez, R.A. (2002) Altern. Ther. Health Med. 8,
(103) Ozgoli, G., Goli, M., & Simbar, M. (2009) J. Altern.
Complement. Med. 15, 243–246. doi:10.1089/acm.2008.0406
(104) Pongrojpaw, D., Somprasit, C., & Chanthasenanont, A. (2007)
J. Med. Assoc. Thai. 90, 1703–1709
(105) Smith, C., Crowther, C., Willson, K., Hotham, N., &
McMillian, V. (2004) Obstet. Gynecol. 103, 639–645.
(106) Levine, M.E., Gillis, M.G., Koch, S.Y., Voss, A.C.,
Stern, R.M., & Koch, K.L. (2008) J. Altern. Complement. Med.
14, 545–551. doi:10.1089/acm.2007.0817
(51) Yeoh, K.G., Kang, J.Y., Yap, I., Guan, R., Tan, C.C., We, A., &
Teng, C.H. (1995) Dig. Dis. Sci. 40, 580–583
(52) Mózsik, G., Szolcsnyi, J., & Rcz, I. (2005) World J.
Gastroenterol. 11, 5180–5184. doi:10.3748/wjg.v11.i33.5180
(53) Satyanarayana, M.N. (2006) Crit. Rev. Food Sci. Nutr. 46,
275–328. doi:10.1080/1040-830491379236
(54) Grossi, L., Cappello, G., & Marzio, L. (2006)
Neurogastroenterol Motil. 18, 632–636. doi:10.1111/j.1365-
(55) Bergonzelli, G.E., Donnicola, D., Porta, N., & Corthésy-
Theulaz, I.E. (2003) Antimicrob. Agents Chemother. 47,
3240–3246. doi:10.1128/AAC.47.10.3240-3246.2003
(56) Lai, P.K., & Roy, J. (2004) Curr. Med. Chem. 11, 1451–1460.
(57) Tremaroli, V., & Bäckhed, F. (2012) Nature 489, 242–249.
(58) Turnbaugh, P.J., Ley, R.E., Mahowald, M.A., Magrini, V.,
Mardis, E.R., & Gordon, J.I. (2006) Nature 444, 1027–1031.
(59) Ley, R.E., Turnbaugh, P.J., Klein, S., & Gordon, J.I. (2006)
Nature 444, 1022–1026. doi:10.1038/4441022a
(60) Karlsson, F.H., Tremaroli, V., Nookaew, I., Bergström, G.,
Behre, C.J., Fagerberg, B., Nielsen, J., & Bäckhed., F. (2013)
Nature 498, 99–103. doi:10.1038/nature12198
(61) Qin, N., Yang, F., Li, A., Prifti, E., Chen, Y., Shao, L., Guo, J.,
Le Chatelier, E., Yao, J., W, J., Zhou, J., Ni, S., Liu, L., Pons, N.,
Batto, J.M., Kennedy, S.P., Leonard, P., Yuan, C., Ding, W., Chen, Y.,
Hu, Z., Zheng, B., Qian, G., Xu, W., Ehrlich, S.D., Zheng, S., &
Li, L. (2014) Nature 513, 59–64. doi:10.1038/nature13568
(62) Karlsson, F.H., Fåk, F., Nookaew, I., Tremaroli, V.,
Fagerberg, B., Petranovic, D., Bäckhed, D., & Nielsen, J. (2012)
Nat. Commun. 3, 1245. doi:10.1038/ncomms2266
(63) Kang, C., Zhang, Y., Zhu, X., Liu, K., Wang, X., Chen, M.,
Wang, J., Chen, H., Hui, S., Huang, L., Zhang, Q., Zhu, J.,
Wang, B., & Mi, M. (2016) J. Clin. Endocrinol. Metab. 101,
4681–4689. doi:10.1210/jc.2016-2786
(64) Hariri, M., & Ghiasvand, R. (2016) Adv. Exp. Med. Biol. 929,
1–24. doi:10.1007/978-3-319-41342-6_1
(65) Fabio, A., Cermelli, C., Fabio, G, Nicoletti, P., & Quaglio, P.
(2007) Phytother. Res. 21, 374–377. doi:10.1002/ptr.1968
(66) Azumi, S., Tanimura, A., & Tanamoto, K. (1997) Biochem.
Biophys. Res. Commun. 234, 506–510. doi:10.1006/bbrc.1997.6668
(67) Rosti, L., & Gastaldi, G. (2005) Pediatrics 11 6, 1057.
(68) Tabak, M., Armon, R., & Neeman, I. (1999) J. Ethnopharmacol.
67, 269–277. doi:10.1016/S0378-8741(99)00054-9
(69) Cao, H., Urban, J.F., Jr, & Anderson, R.A. (2008) J. Nutr. 138,
833–840. doi:10.1093/jn/138.5.833
(70) Kim, D.H., Kim, C.H., Kim, M.S., Kim, J.Y., Chung, J.H.,
Lee, J.W., Yu, B.P., & Chung, H.Y. (2007) Biogerontology 8,
545–554. doi:10.1007/s10522-007-9098-2
(71) Roussel, A.M., Hininger, I., Benaraba, R., Ziegenfuss, T.N., &
Anderson, R.A. (2009) J. Am. Coll. Nutr. 28, 16–21
(72) Preuss, H.G., Echard, B., Polansky, M.M., & Anderson, R.
(2006) J. Am. Coll. Nutr. 25, 144–150
(73) Huang, J., Wang, S., Luo, X., Xie, Y., & Shi, X. (2007) Thromb.
Res. 119 , 337–342. doi:10.1016/j.thromres.2006.03.001
(74) Qin, B., Dawson, H., Polansky, M.M., & Anderson, R.A. (2009)
Horm. Metab. Res. 41, 516–522
(75) Tuzcu, Z., Orhan, C., Sahin, N., Juturu, V., & Sahin, K. (2017)
Oxid. Med. Cell. Longevity 2017. doi:10.1155/2017/1583098
(76) Byrne, A., Makadia, S., Sutherland, A., & Miller, M.
(2017) Arch. Med. Res. 48, 483–487. doi:10.1016/j.
(77) Maierean, S.M., Serban, M.C., Sahebkar, A., Ursoniu, S.,
Serban, A., Penson, P., & Banach, M.; Lipid and Blood Pressure
Meta-alaysis Collaboration (LBPMC) Group (2017) J. Clin.
Lipidol. 11, 1393–1406. doi:10.1016/j.jacl.2017.08.004
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 407
(135) Arablou, T., Aryaeian, N., Valizadeh, M., Shari, F.,
Hosseini, A., & Djalali, M. (2014) Int. J. Food Sci. Nutr. 65,
515–520. doi:10.3109/09637486.2014.880671
(136) Shidfar, F., Rajab, A., Rahideh, T., Khandouzi, N.,
Hosseini, S., & Shidfar., S. (2015) J. Complement. Integr. Med.
12, 165–170. doi:10.1515/jcim-2014-0021
(137) Mahluji, S., Attari, V.E., Mobasseri, M., Payahoo, L.,
Ostadrahimi, A., & Golzari, S.E. (2013) Int. J. Food Sci. Nutr.
64, 682–686. doi:10.3109/09637486.2013.775223
(138) Miyamoto, M., Matsuzaki, K., Katakura, M., Hara, T.,
Tanabe, Y., & Shido, O. (2015) Int. J. Biometeorol. 59,
1461–1474. doi:10.1007/s00484-015-0957-2
(139) Mansour, M.S., Ni, Y.M., Roberts, A.L., Kelleman, M.,
Roychoudhury, A., & St-Onge, M.P. (2012) Metabolism 61,
1347–1352. doi:10.1016/j.metabol.2012.03.016
(140) Ebrahimzadeh Attari, V., Ostadrahimi, A., Asghari Jafarabadi, M.,
Mehralizadeh, S., & Mahluki, S. (2016) Eur. J. Nutr. 55,
2129–2136. doi:10.1007/s00394-015-1027-6
(141) Grzanna, R., Phan, P., Polotsky, A., Lindmark, L., &
Fondoza, C.G. (2004) J. Altern. Complement. Med. 10,
1009–1013. doi:10.1089/acm.2004.10.1009
(142) Kim, D.S., Kim, J.Y., & Han, Y.S. (2007) J Altern Complement
Med. 13(3):333-40
(143) Kapoor, I.P., Singh, B., Singh, G., De Heuluani, C.S.,
De Lampasona, M.P., & Catalan, C.A.N. (2009) J. Agric. Food
Chem. 57, 5358–5364. doi:10.1021/jf900642x
(144) Agbor, G.A., Vinson, J.A, Oben, J.E., & Ngogang, J.Y. (2007)
J. Herb. Pharmacother. 7, 49–64
(145) Srinivasan, K. (2007) Crit. Rev. Food Sci. Nutr. 47, 735–748.
(146) Kaleem, M., Sheema, K., Sarmad, H., & Bano, B. (2005)
Indian J. Physiol. Pharmacol. 49, 65–71
(147) Vijayakumar, R.S., & Nalini, N. (2006) Cell. Biochem. Funct.
24, 491–498. doi:10.1002/cbf.1331
(148) Tasleem, F., Azhar, I., Ali, S.N., Perveen, S., & Mahmood, Z.A.
(2014) Asian Pac. J. Trop. Dis. 7, S461–S468. doi:10.1016/
(149) Mujumdar, A.M., Dhuley, J.N., Deshmukh, V.K., Raman, P.H., &
Naik, S.R. (1990) Jpn. J. Med. Sci. Biol. 43, 95–100
(150) Prasad, N.S., Raghavendra, R., Lokesh, B.R., & Naidu, K.A.
(2004) Prostaglandins, Leukotrienes Essent. Fatty Acids 70,
521–528. doi:10.1016/j.plefa.2003.11.006
(151) Stohr, J.R., Xiao, P.G., & Bauer, R. (2001) J Ethnopharmacol
75, 133–139. doi:10.1016/S0378-8741(00)00397-4
(152) Bang, J.S., Ohda, H., Choi, H.M., Sur, B.J., Lim, S.J.,
Kim, J.Y., Yang, H.I., Yoo, M.C., Hahm, D.H., & Kim, K.S.
(2009) Arthritis Res. Ther. 11, R49. doi:10.1186/ar2662
(153) Kumar, S., Singhal, V., Roshan, R., Sharma, A.,
Rembhotkar, G.W., & Ghosh, B. (2007) Eur. J. Pharmacol.
575, 177–186. doi:10.1016/j.ejphar.2007.07.056
(154) Pradeep, C.R., & Kuttan, G. (2004) Int. Immunopharmacol. 4,
1795–1803. doi:10.1016/j.intimp.2004.08.005
(155) Bae, G.S., Kim, M.S., Jung, W.S., Seo, S.W., Yun, S.W., Kin, S.G.,
Park, R.K., Kim, E.C., Song, H.J., & Park, S.J. (2010) Eur. J.
Pharmacol. 642, 154–162. doi:10.1016/j.ejphar.2010.05.026
(156) Delecroix, B., Abaïdia, A.E., Leduc, C., Dawson, B., &
Dupont, G. (2017) J. Sports Sci. Med. 16, 147–153
(157) Kim, S.H., & Lee, Y.C. (2009) J. Pharm. Pharmacol. 61,
353–359. doi:10.1211/jpp/61.03.0010
(158) Platel, K., & Srinivasan, K. (2004) Indian J. Med. Res. 119 ,
(159) Matsuda, D., Ohte, S., Ohshiro, T., Jiang, W., Rudel, L.,
Hong, B., Si, S., & Tomoda, H. (2008) Biol. Pharm. Bull. 31,
(160) Vijayakumar, R.S., & Nalini, N. (2006) J. Basic Clin. Physiol.
Pharmacol. 17, 71–86
(161) Lee, K.P., Lee, K., Park, W.H., Kim, H., & Hong, H. (2015)
J. Med. Food 18, 208–15. doi:10.1089/jmf.2014.3229
(107) Bameshki, A., Namaiee, M.H., Jangjoo, A., Dadgarmoghaddam, M.,
Ghalibaf, M.H.E., Ghorbanzadeh, A., & Sheybani, S. (2018)
Electron. Physician. 10, 6354–6362. doi:10.19082/6354
(108) Dabaghzadeh, F., Khalili, H., Dashti-Khavidaki, S.,
Abbasian, L., Moeinifard, A. (2014) Expert Opin. Drug Saf. 13,
859–866, doi:10.1517/14740338.2014.914170
(109) Zick, S.M., Rufn, M.T., Lee, J., Normolle, D.P., Siden, R.,
Alrawi, S., & Brenner, D.E. (2009) Support Care Cancer 17,
563–572. doi:10.1007/s00520-008-0528-8
(110) Woo, H.M., Kang, J.H., Kawada, T., Yoo, H., Sung, M.K., &
Yu, R. (2007) Life Sci. 80, 926–931. doi:10.1016/j.lfs.2006.11.030
(111) Jung, H.W., Yoon, C.H., Park, K.M., Han, H.S., & Park, Y.K.
(2009) Food Chem. Toxicol. 47, 1190–1197. doi:10.1016/j.
(112) Dugasani, S., Pichika, M.R., Nadarajah, V.D., Balijepalli, M.K.,
Tandra, S., & Korlakunta, J.N. (2009) J. Ethnopharmacol. 127,
515–520. doi:10.1016/j.jep.2009.10.004
(113) Ahn, S.I., Lee, J.K., & Youn, H.S. (2009) Mol. Cells. 27,
211–215. doi:10.1007/s10059-009-0026-y
(114) Sang, S., Hong, J., Wu, H., Liu, J., Yang, C.S., Pan, M.H.,
Badamaev, V., & Ho, C.T. (2009) J. Agric. Food Chem. 57,
10645–10650. doi:10.1021/jf9027443
(115) Mozaffari-Khosravi, H., Naderi, Z., Dehghan, A.,
Nadjarzadeh, A., & Fallah Huseini, H. (2016) J. Nutr. Gerontol.
Geriatr. 35, 209–218. doi:10.1080/21551197.2016.1206762
(116) Jiang, Y., Turgeon, D.K., Wright, B.D., Sidahmed, E.,
Rufn, M.T., Brenner, D.E., Sen, A., & Zick, S.M. (2013) Eur. J.
Cancer Prev. 22, 455–460. doi:10.1097/CEJ.0b013e32835c829b
(117) Nicoll, R., & Henein, M.Y. (2009) Int. J. Cardiol. 131, 408–409.
(118) Chrubasik, S., Pittler, M.H., & Roufogalis, B.D. (2005)
Phytomedicine 12, 684–670. doi:10.1016/j.phymed.2004.07.009
(119) Ghayur, M.N., Gilani, A.H., & Afridi, M.B. (2005) Vascul
Pharmacol. 43(4):234-41
(120) Alizadeh-Navaei, R., Roozbeh, F., Saravi, M., Pouramir, M.,
Jalali, F., & Moghadamnia, A.A. (2008) Saudi Med. J. 29, 1280–1284
(121) Bordia, A., Verma, S.K., & Srivastava, K.C. (1997)
Prostaglandins, Leukotrienes Essent. Fatty Acids 56, 379–384.
(122) Lumb, A.B. (1994) Thromb. Haemost. 71, 110–111
(1 23) Young, H.Y., Liao, J.C., Chang, Y.S., Luo, Y.L., Lu, M.S., & Peng, W.H.
(2006) Am. J. Chin. Med. 34, 545–551. doi:10.1142/S0192415X06004089
(124) Han, L.K., Morimoto, C., Zheng, Y.N., Li, W., Asami, E.,
Okuda, H., & Saito, M. (2008) Yakugaku Zasshi. 128, 1195–1201.
(125) Fouda, A.M., & Berika, M.Y. (2009) Basic Clin. Pharmacol.
Toxicol. 104, 262–271. doi:10.1111/j.1742-7843.2008.00363.x
(126) Funk, J.L., Frye, J.B., Oyarzo, J.N., & Timmermann, B.N.
(2009) J. Nat. Prod. 27, 403–407. doi:10.1021/np8006183
(127) Black, C.D., Herring, M.P., Hurley, D.J., & O’Connor, P. (2010)
J. Pain 11, 894–903
(128) Matsumura, M.D., Zavorsky, G.S., & Smoliga, J.M. (2015)
Phytother. Res. 29, 887–893. doi:10.1002/ptr.5328
(129) Saraswat, M., Reddy, P.Y., Muthenna, P., & Reddy, G.B. (2009)
Br. J. Nutr. 101, 1714–1721. doi:10.1017/S0007114508116270
(130) Dearlove, R.P., Greenspan, P., Hartle, D.K., Swanson, R.B., &
Hargrove, J.L. (2008) J. Med. Food. 11, 275–281. doi:10.1089/
(131) Al-Amin, Z.M., Thomson, M., Al-Qattan, K.K.,
Peltonen-Shalaby, R., & Ali, M. (2006) Br. J. Nutr. 96,
660–666. doi:10.1079/BJN20061849
(132) Bhandari, U., Kanojia, R., & Pillai, K.K. (2005)
J. Ethnopharmacol. 97, 227–230. doi:10.1016/j.jep.2004.11.011
(133) Nammi, S., Sreemantula, S., & Roufogalis, B.D. (2009)
Basic Clin. Pharmacol. Toxicol. 104, 366–373. doi:10.1111/
(134) Ojewole, J.A. (2006) Phytother. Res. 20, 764–772. doi:10.1002/
408 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
(186) Rahmani, S., Asgary, S., Askar, G., Keshvari, M.,
Hataminpour, M., Feizi, A., & Sahebkar, A. (2016) Phytother.
Res. 30, 1540–1548. doi:10.1002/ptr.5659
(187) Gongadze, N., Antelava, N., & Kezeli, T. (2008) Georgian Med.
News. 155, 44–48
(188) Yang, F., Lim, G.P., Begum, A.N., Ubeda, O.J., Simmons, M.R.,
Ambegaokar, S.S., Chen, P.P., Kayed, R., Glabe, C.G.,
Frautschy, S.A., & Cole, G.M. (2005) J. Biol. Chem. 280,
5892–5901. doi:10.1074/jbc.M404751200
(189) Cashman, J.R., Ghirmai, S., Abel, K.J., & Fiala, M. (2008) BMC
Neurosci. 9, S13. doi:10.1186/1471-2202-9-S2-S13
(190) Ahmed, T., & Gilani, A.H. (2009) Pharmacol. Biochem. Behav.
91, 554–559. doi:10.1016/j.pbb.2008.09.010
(191) Ishrat, T., Hoda, M.N., Khan, M.B., Yousuf, S., Ahmad, M.,
Khan, M.M., Ahmad, A., & Islam, F. (2009) Eur. Neuropsycho-
pharmacol. 19, 636–647. doi:10.1016/j.euroneuro.2009.02.002
(192) Wakade, C., King, M.D., Laird, M.D., Alleyne, C.H., Jr, &
Dhandapani, K.M. (2009) Antioxid. Redox. Signal. 11, 35–45.
(193) Ng, T.P., Chiam, P.C., Lee, T., Chua, H.C., Lim, L., & Kua, E.H.
(2006) Am. J. Epidemiol. 164, 898–906. doi:10.1093/aje/kwj267
(194) Rainey-Smith, S.R., Brown, B.M., Sohrabi, H.R., Shah, T.,
Goozee, K.G., Gupta, V.B., & Martins, R.N. (2016) Br. J. Nutr.
115 , 2106–2113. doi:10.1017/S0007114516001203
(195) Yu, J.J., Pei, L.B., Zhang, Y., Wen, Z.Y., & Yang, J.L. (2015)
J. Clin. Psychopharmacol. 35, 406–410. doi:10.1097/
(196) Park, C., Moon, D.O., Choi, I.W., Choi, B.T., Nam, T.J., Rhu, C.H.,
Kwon, T.K., Lee, W.H., Kim, G.Y., & Choi, Y.H. (2007) Int. J.
Mol. Med. 20, 365–372. doi:10.3892/ijmm.20.3.365
(197) Funk, J.L., Oyarzo, J.N., Frye, J.B., Chen, G., Lantz, R.C.,
Sólyom, A.M., & Timmermann, B.N. (2006) J. Nat. Prod. 69,
351–355. doi:10.1021/np050327j
(198) Panahi, Y., Alishiri, G.H., Parvin, S., & Sahebkar, A. (2016) J.
Diet Suppl. 13, 209–220. doi:10.3109/19390211.2015.1008611
(199) Amalraj, A., Varma, K., Jacob, J., Divya, C.,
Kunnumakkara, A.B., Stohs, S.J., & Gopi, S. (2017) J. Med.
Food. 20, 1022–1030. doi:10.1089/jmf.2017.3930
(200) Kuptniratsaikul, V., Thanakhumtorn, S., Chinswangwantanakul, P.,
Wattanamongkonsil, L., & Thamlikitkul, V. (2009) J. Altern.
Complement. Med. 15, 891–897. doi:10.1089/acm.2008.0186
(201) Haroyan, A., Mukuchyan, V., Mkrtchyan, N., Minasyan, N.,
Gasparyan, S., Sargsyan, A., Narimanyan, M., &
Hovhannisyan, A. (2018) BMC Complement. Altern. Med. 18, 7
(202) Kim, T., Davis, J., Zhang, A.J., He, X., & Matthews, S.T. (2009)
Biochem. Biophys. Res. Commun. 388, 377–382. doi:10.1016/j.
(203) Wang, S.L., Li, Y., Wen, Y., Chen, Y.F., Na, L.X., Li, S.T., &
Sun, C.H. (2009) Biomed. Environ. Sci. 22, 32–9. doi:10.1016/
(204) Best, L., Elliott, A.C., & Brown, P.D. (2007) Biochem.
Pharmacol. 73, 1768–1775. doi:10.1016/j.bcp.2007.02.006
(205) Cheng, T.C., Lin, C.S., Hsu, C.C., Chen, L.J., Cheng, K.C., &
Cheng, J.T. (2009) Neurosci. Lett. 465, 238–241. doi:10.1016/j.
(206) Usharani, P., Mateen, A.A., Naidu, M.U., Raju, Y.S., &
Chandra, N. (2008) Drugs R. D. 9, 243–250
(207) Navekar, R., Rafraf, M., Ghaffari, A., Asghari-Jafarabadi, M., &
Khoshbaten, M. (2017) J. Am. Coll. Nutr. 36, 261–267. doi:10.1
(208) Di Pierro, F., Bressan, A., Ranaldi, D., Rapacioli, G.,
Giacomelli, L., & Bertucciloli, A. (2015) Eur. Rev. Med.
Pharmacol. Sci. 19, 4195–4202
(209) Panahi, Y., Kianpour, P., Mohtashami, R., Jafari, R., Simental-
Mendía, L.E., & Sahebkar, A. (2017) Drug Res (Stuttg.) 67,
244–251. doi:10.1055/s-0043-100019
(162) Taqvi, S.I., Shah, A.J., & Gilani, A.H. (2008) J. Cardiovasc.
Pharmacol. 52, 452–458. doi:10.1097/FJC.0b013e31818d07c0
(163) Westerterp-Plantenga, M., Diepvens, K., Joosen, A.M., Bérubé-
Parent, S., & Tremblay, A. (2006) Physiol Behav. 89 85–91.
(164) Zanzer, Y.C., Plaza, M., Dougkas, A., Turner, C., & Östman, E.
(2018) Food Funct. 9, 2774–2786. doi:10.1039/C7FO01715D
(165) Khajuria, A., Zutshi, U., & Bedi, K. (1998) Ind. J. Exp. Biol. 36,
(166) Khajuria, A., Thusu, N., & Zutshi, U. (2002) Phytomedicine 9,
224–231. doi:10.1078/0944-7113-00114
(167) Shoba, G., Joy, D., Joseph, T., Majeed, M., Rajendran, R., &
Srinivas, P.S. (1998) Planta Med. 64, 353–356.
(168) Rinwa, P., & Kumar, A. (2012) Brain Res. 1488, 38–50.
(169) Johnson, J.J., Nihal, M., Siddiqui, I.A., Scarlett, C.O.,
Bailey, H.H., Mukhtar, H., & Ahmad, N. (2011) Mol. Nutr. Food
Res. 55, 1169–1176. doi:10.1002/mnfr.201100117
(170) Li, S., Wan, C., Wang, M., Li, W., Matsumoto, K., & Tang, Y.
(2007) Life Sci. 80, 1373–1381. doi:10.1016/j.lfs.2006.12.027
(171) Wattanathorn, J., Chonpathompikunlert, P., Muchimapura, S.,
Priprem, A., & Tankamnerdthai, O. (2008) Food Chem. Toxicol.
46, 3106–3110. doi:10.1016/j.fct.2008.06.014
(172) Panahi, Y., Hosseini, M.S., Khalili, N., Simental-Mendía, M., &
Sahebkar, A. (2016) Biomed. Pharmacother. 82, 578–582.
(173) Srivastava, G., & Mehta, J.L. (2009) J. Cardiovasc. Pharmacol.
Ther. 14, 22–27. doi:10.1177/1074248408329608
(174) Fang, X.D., Yang, F., Zhu, L., Shen, Y.L., Wang, L.L., &
Cheng, Y.Y. (2009) Clin. Exp. Pharmacol. Physiol. 36, 1177–1182
(175) Soni, K.B., & Kuttan, R. (1992) Indian J. Physiol. Pharmacol.
36, 273–275
(176) Alwi, I., Santoso, T., Suyono, S., Sutrisna, B., Suyatna, F.D.,
Kresno, S.B., & Ernie, S. (2008) Acta Med. Indones. 40, 201–210
(177) Panahi, Y., Khalili, N., Sahebi, E., Namazi, S., Reiner, Ž.,
Majeed, M., & Sahebkar, A. (2017) Complement. Ther. Med. 33,
1–5. doi:10.1016/j.ctim.2017.05.006
(178) Santos-Parker, J.R., Strahler, T.R., Bassett, C.J., Bispham, N.Z.,
Chonchol, M.B., & Seals, D.R. (2017) Aging (Albany NY) 9,
187–208. doi:10.18632/aging.101149
(179) Panahi, Y., Hosseini, M.S., Khalili, N., Naimi, E., Soaei, S.S.,
Majed, M., & Sahebkar, A. (2016) Nutrition 32(10):1116–1122.
(180) Bundy, R., Walker, A.F., Middleton, R.W., & Booth, J. (2004)
J. Altern. Complement. Med. 10, 1015–1018. doi:10.1089/
(181) Hanai, H., Lida, T., Takeuchi, K., Wanatabe, F., Maruyama, Y.,
Andoh, A., Tsujikawa, T., Kuujiyama, Y., Mitsuyama, K.,
Sata, M., Yamada, M., Iwaoka, Y., Kanke, K., Hirashi, H.,
Hirayama, K., Arai, H., Yoshii, S., Uchijima, M., Nagata, T., &
Koide, Y. (2006) Clin. Gastroenterol. Hepatol. 4, 1502–1506.
(182) De, R., Kundu, P., Swarnakar, S., Ramamurthy, T.,
Chowdhury, A., Nair, G.B., & Mukhopadhyay, A.K. (2009)
Antimicrob. Agents Chemother. 53, 1592–1597. doi:10.1128/
(183) Zaidi, S.F., Yamada, K., Kadowaki, M., Usmanghani, K., &
Sugiyama, T. (2009) J. Ethnopharmacol. 121, 286–291.
(184) Khonche, A., Biglaria, O., Panahi, Y., Valizadegan, G., Soaei, S.S.,
Ghamarchehreh, M.E., Majeed, M., & Sahebkar, A. (2016) Drug
Res. (Stuttg.) 66, 444–448. doi:10.1055/s-0042-109394
(185) Panahi, Y., Kianpour, P., Mohtashami, R., Jafari, R.,
Simental-Mendía, L.E., & Sahebkar, A. (2016) J. Cardiovasc.
Pharmacol. 68, 223–229. doi:10.1097/FJC.0000000000000406
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 409
(236) Rao, A., Steels, E., Beccaria, G., Inder, W.J., & Vitetta, L.
(2015) Phytother. Res. 29, 1123–1130. doi:10.1002/ptr.5355
(237) Rao, A., Steels, E., Inder, W.J., Abraham, S., & Vitetta, L. (2016)
Aging Male. 19, 134–142. doi:10.3109/13685538.2015.1135323
(238) Maheshwari, A., Verma, N., Swaroop, A., Bagchi, M.,
Preuss, H.G., Tiwari, K., & Bagchi, D. (2017) Int. J. Med. Sci.
14, 58–66. doi:10.7150/ijms.17256
(239) Steels, E., Ra, A., & Vitetta, L. (2011) Phytother. Res. 25,
1294–1300. doi:10.1002/ptr.3360
(240) Wilborn, C., Taylor, L., Poole, C., Foster, C., Willoughby, D., &
Kreider, R. (2010) Int. J. Sport Nutr. Exerc. Metab. 20, 457–465
(241) Aruoma, O.I., Halliwell, B., & Aeschbach, R. (1992) Xenobiotica.
(242) Wijeratne, S.S.K., & Cuppett, S.L. (2007) J. Agric. Food Chem.
55, 1193–1199. doi:10.1021/jf063089m
(243) Posadas, S.J., Caz, V., Largo, C., De la Gnadara, B.,
Matallanas, B., Reglero, G., & De Miguel, E. (2009) Exp.
Gerontol. 44, 383–389. doi:10.1016/j.exger.2009.02.015
(244) Huang, H.C., Huang, C.Y., Lin-Shiau, S.Y., & Lin, J.K. (2009)
Mol. Carcinog. 48, 517–531. doi:10.1002/mc.20490
(245) Colica, C., Di Renzo, L., Aiello, V., De Lorenzo, A., &
Abenavoli, L. (2018) Rev. Recent Clin. Trials 13, 240–242.
(246) Moss, M., Cook, J., Wesnes, K., & Duckett, P. (2003) Int. J.
Neurosci. 113, 15–38
(247) McCaffrey, R., Thomas, D.J., & Kinzelman, A.O. (2009) Holist.
Nurs. Pract. 23, 88–93. doi:10.1097/HNP.0b013e3181a110aa
(248) Machado, D.G., Bettio, L.E., & Cunha, M.P. (2009) Prog.
Neuropsychopharmacol. Biol. Psychiatry 33, 642–650.
(249) Adsersen, A., Gauguin, B., Gudiksen, L., & Jäger, A.K.
(2006) J. Ethnopharmacol. 104, 418–422. doi:10.1016/j.
(250) Orhan, I., Aslan, S., Kartal, M., Sener, B., & Hüsnü Can
Başer, K. (2008) Food Chem.108, 663–668. doi:10.1016/j.
(251) Kim, S.J., Kim, J.S., Cho, H.S., Lee, H.J., Kim, S.Y., Kim, S.,
Lee, S.Y., & Chun, H.S. (2006) Neuroreport 17, 1729–1733.
(252) Park, J.A., Kim, S., Lee, S.Y., Kim, C.s., Kim, D.K., Kim, S.J., &
Chun, H.S. (2008) Neuroreport 19, 1301–1304. doi:10.1097/
(253) Satoh, T., Kosaka, K., Itoh, K., Kobayashi, A., Yamamoto, M.,
Shimojo, Y., Kitajima, C., Cui, J., Kamins, J., Okamoto, S.,
Izumi, M., Shirasawa, T., & Lipton, S.A. (2008) J. Neurochem.
104, 1116–1131. doi:10.1111/j.1471-4159.2007.05039.x
(254) Pearson, D.A., Frankel, E.N., Aeschbach, R., & German, J.B.
(1997) J. Agric. Food Chem. 45, 578–582. doi:10.1021/jf9603893
(255) Lee, J.J., Jin, Y.R., Lee, J.H., Yu, J.Y., Han, X.H., Oh, K.W.,
Hong, J.T., Kim, T.J., & Yun, Y.P. (2007) Planta Med. 73,
121–127. doi:10.1055/s-2006-957066
(256) Naemura, A., Ura, M., Yamashita, T., Arai, R., &
Yamamoto, J. (2008) Thromb. Res. 122, 517–522. doi:10.1016/j.
(257) Kwon, Y.I., Vattem, D.A., & Shetty, K. (2006) Asia Pac. J. Clin.
Nutr. 15, 107–118
(258) Bakirel, T., Bakirel, U., Keleş, O.U., Ülgen, S.G., & Yardibi, H.
(2008) J. Ethnopharmacol. 11 6, 64–73. doi:10.1016/j.
(259) Rau, O., Wurglics, M., Paulke, A., Zitzkowski, J.,
Meindl, N., Bock, A., Dingermann, T., Abdel-Tawab, M., &
Schubert-Zsilavecz, M. (2006) Planta Med. 72, 881–887.
(260) Ercan, P., & El, S.N. (2018) Int. J. Biol. Macromol. 115 ,
933–939. doi:10.1016/j.ijbiomac.2018.04.139
(210) Kunnumakkara, A.B., Anand, P., & Aggarwal, B.B. (2008)
Cancer Lett. 269, 199–225. doi:10.1016/j.canlet.2008.03.009
(211) Dhillon, N., Aggarwal, B.B., Newman, R.A., Wolff, R.A.,
Kunnumakkara, A.B., Abbruzzese, J.L., Ng, C.S.,
Badmaev, V., & Kurzrock, R. (2008) Clin Cancer Res. 14,
4491–4499. doi:10.1158/1078-0432.CCR-08-0024
(212) Petit, P.R., Sauvaire, Y.D., Hillaire-Buys, D.M., Leconte, O.M.,
Baissac, Y.G., Ponsin, G.R., & Ribes, G.R. (1995) Steroids 60,
674–680. doi:10.1016/0039-128X(95)00090-D
(213) Boban, P.T., Nambisan, B., & Sudhakaran, P.R. (2006) Br. J.
Nutr. 96, 1021–1029.
(214) Srichamroen, A., Field, C.J., Thomson, A.B., & Basu, T.K. (2008)
J. Clin. Biochem. Nutr. 43, 167–174. doi:10.3164/jcbn.2008060
(215) Narender, T., Puri, A., Shweta, A., Khaliq, T., Saxena, R.,
Bhatia, G., & Chandra, R. (2006) Bioorg. Med. Chem. Lett. 16,
293–296. doi:10.1016/j.bmcl.2005.10.003
(216) Sowmya, P., & Rajyalakshmi, P. (1999) Plant Foods Hum. Nutr.
53, 359–365
(217) Chevassus, H., Gaillard, J.B., Farret, A., Costa, F., Gabillaud, I.,
Mas, E., Dupuy, A.M., Michel, F., Cantié, C., Renard, E.,
Galtier, F., & Petit, P. (2010) Eur. J. Clin. Pharmacol. 66,
449–55. doi:10.1007/s00228-009-0770-0
(218) Jetté, L., Harvey, L., Eugeni, K., & Lvens, N. (2009) Curr.
Opin. Investig. Drugs 10, 353–358
(219) Kannappan., S., & Anuradha, C.V. (2009) Indian J. Med. Res.
129, 401–408
(220) Hannan, J.M., Ali, L., Rokeya, B., Khaleque, J., Akhter, M.,
Flatt, P.R., & Abdl-Wahab, Y.H. (2007) Br. J. Nutr. 97, 514–521.
(221) Srichamroen, A., Thomson, A.B., Field, C.J., & Basu, T.K.
(2009) Nutr Res. 29, 49–54. doi:10.1016/j.nutres.2008.11.002
(222) Gopalpura, P.B., Jayanthi, C., & Dubey, S. (2007) Int. J.
Diabetes Dev. Ctries. 27, 4145
(223) Robert, S.D., Ismail, A.A., & Rosli, W.I. (2016) Eur. J. Nutr. 55,
2275–2280. doi:10.1007/s00394-015-1037-4
(224) Rafraf, M., Malekiyan, M., Asghari-Jafarabadi, M., &
Aliasgarzadeh, A. (2014) Int. J. Vitam. Nutr. Res. 84, 196–205.
(225) Handa, T., Yamaguchi, K., Sono, Y., & Yazawa, K. (2005) Biosci.
Biotechnol. Biochem. 69, 1186–1188. doi:10.1271/bbb.69.1186
(226) Mathern, J.R., Raatz, S.K., Thomas, W., & Slavin, J.L. (2009)
Phytother. Res. 23, 1543–1548. doi:10.1002/ptr.2795
(227) Chevassus, H., Molinier, N., Costa, F., Gabillaud, I.,
Mas, E., Dupuy, A.M., Michel, F., Cantié, C., Renard, E.,
Galtier, F., & Petit, P. (2010) Eur. J. Clin. Pharmacol. 66,
449–455. doi:10.1007/s00228-009-0770-0
(228) Ruby, B.C., Gaskill, S.E., Slivka, D., & Harger, S.G. (2005)
Amino Acids 28, 71–76. doi:10.1007/s00726-004-0143-z
(229) Slivka, D., Cuddy, J., Hailes, W., Harger, S., & Ruby, B. (2008)
Amino Acids 35, 439–444. doi:10.1007/s00726-007-0580-6
(230) Ikeuchi, M., Yamaguchi, K., Koyama, T., Sono, Y., &
Yazawa, K. (2006) J. Nutr. Sci. Vitaminol. (Tokyo) 52, 287–292.
(231) Kaviarasan, S., Sundarapandiyan, R., & Anuradha, C.V. (2008)
Cell Biol. Toxicol. 24, 391–400. doi:10.1007/s10565-007-9050-x
(232) Reddy, R.L., & Srinivasan, K. (2009) Can. J. Physiol.
Pharmacol. 87, 684–693. doi:10.1139/y09-062
(233) Raju, J., & Bird, R.P. (2006) Int. J. Obes. (Lond.) 30, 1298–
1307. doi:10.1038/sj.ijo.0803254
(234) Steels, E., Steele, M.L., Harold, M., & Coulson, S. (2017)
Phytother. Res. 31, 1316–1322. doi:10.1002/ptr.5856
(235) Shamshad Begum, S., Jayalakshmi, H.K., Vidyavathi, H.G.,
Gopakumar, G., Abin, I., Balu, M., Geetha, K., Suresha, S.V.,
Vasundhara, M., & Krishnakumar, I.M. (2016) Phytother. Res.
30, 1775–1784. doi:10.1002/ptr.5680
410 Jiang: Journal of aoaC international Vol. 102, no. 2, 2019
(285) Szulińska, M., Kręgielska-Narożna, M., Świątek, J., Styś, P.,
Kuźnar-Kamińska, B., Jakubowski, H., Walkowiak, J., &
Bogdański, P. (2018) Biomed. Pharmacother. 102, 792–797.
(286) Mahdavi-Roshan, M., Zahedmehr, A., Mohammad-Zadeh, A.,
Sanati, H.R., Shakerian, F., Firouzi, A., Kiani, R., &
Nasrollahzadeh, J. (2013) Nutr. Health 22, 143–155.
(287) Rai, S.K., Sharma, M., & Tiwari, M. (2009) Life Sci. 85,
211–219. doi:10.1016/j.lfs.2009.05.020
(288) Reinhart, K.M., Talati, R., White, C.M., & Coleman, C.I.
(2009) Nutr Res Rev. 22, 39–48. doi:10.1017/
(289) Varshney, R., & Budoff, M.J. (2016) J. Nutr. 146, 416S–421S.
(290) Mahdavi-Roshan, M., Nasrollahzadeh, J.,
Mohammad Zadeh, A., & Zahedmehr, A. (2016) Iran. Red
Crescent Med. J. 18, e23871. doi:10.5812/ircmj.23871
(291) Oboh, G., Ademiluyi, A.O., Agunloye, O.M., Ademosun, A.O., &
Ogunsakin, B.G. (2018) J. Diet. Suppl. 9, 1–14. doi:10.1080/19
(292) Al-Qattan, K.K., Thomson, M., Al-Mutawa’a, S., Al-Hajeri, D.,
Drobiova, H., & Ali, M. (2006) J. Nutr. 136, 774S–776S.
(293) Lei, Y.P., Liu, C.T., Sheen, L.Y., Chen, H.W., & Lii, C.K.
(2010) Mol. Nutr. Food Res. 54, S42–S52. doi:10.1002/
(294) Hosseini, M., Shaee, S.M., & Baluchnejadmojarad, T.
(2007) Pathophysiology 14, 109–112. doi:10.1016/j.
(295) Benavides, G., Squadrito, G.L., Mills, R.W., Patel, H.D.,
Isbell, T.S., Patel, R.P., Darley-Usmar, V.M., Doeller, J.E., &
Krauss, D.W. (2007) Proc. Natl. Acad. Sci. U S A 104,
17977–17982. doi:10.1073/pnas.0705710104
(296) Reinhart, K.M., Coleman, C.I., Teevan, C., Vachhani, P., &
White, C.M. (2008) Ann. Pharmacother. 42, 1766–1771.
(297) Rahman, K. (2007) Mol. Nutr. Food. Res. 51, 1335–1344.
(298) Steiner, M., & Li, W. (2001) J. Nutr. 131, 980S–984S.
(299) Fukao, H., Yoshida, H., Tazawa, Y., & Hada, T. (2007) Biosci.
Biotechnol. Biochem. 71, 84–90. doi:10.1271/bbb.60380
(300) Hiyasat, B., Sabha, D., Grotzinger, K., Kempfert, J.,
Rauwalk, J.W., Mohr, F.W., & Dhein, S. (2009) Pharmacology
83, 197–204. doi:10.1159/000196811
(301) Pierre, S., Crosbie, L., & Duttaroy, A.K. (2005) Platelets 16,
469–473. doi:10.1080/09537100500129540
(302) Scharbert, G., Kalb, M.L., Duris, M., Marschalek, C., &
Kozek-Langenecker, S.A. (2007) Anesth. Analg. 105, 1214–
1218. doi:10.1213/01.ane.0000287253.92211.06
(303) Wojcikowski, K., Myers, S., & Brooks, L. (2007) Platelets 18,
29–34. doi:10.1080/09537100600800636
(304) Womack, C.J., Lawton, D.J., Redmond, L., Todd, M.K., &
Hargens, T.A. (2015) J. Int. Soc. Sports Nutr. 12, 23.
(305) Drobiova, H., Thomson, M., Al-Qattan, K.,
Peltonen-Shalaby, R., Al-Amin, Z., & Ali, M. (2011)
Evid. Based Complement. Alternat. Med. 2011, 703049.
(306) Jalal, R., Bagheri, S.M., Moghimi, A., & Rasuli, M.B.
(2007) J. Clin. Biochem. Nutr. 41:218–223. doi:10.3164/
(307) Liu, C.T., Wong, P.L., Lii, C.K., Hse, H., & Sheen, L.Y.
(2006) Food Chem. Toxicol. 44, 1377–1384. doi:10.1016/j.
(261) Hsieh, C.L., Peng, C.H., Chyau, C.C., Lin, Y.C., Wang, H.W., &
Peng, R.Y. (2007) J Agric Food Chem. 55, 2884–2891.
(262) Martin, R., Pierrard, C., Lejeune, F., Hilaire, P., Breton, L., & Bererd, F.
(2008) Eur. J. Dermatol. 18, 128–135. doi:10.1684/ejd.2008.0349
(263) Calabrese, V., Scapagnini, G., Catalano, C., Dinotta, F.,
Geraci, D., & Morganti, P. (2000) Int. J. Tissue React. 22, 5–1
(264) Galisteo, M., Surez, A., Montilla, M.P., Torres, M.I.,
Gil, A., & Navarro, M.C. (2006) Phytomedicine. 13, 101–108.
(265) Harach, T., Aprikian, O., Monnard, I., Moulin, J., Membrez, M.,
Bélor, J.C., Raab, T., Macé, K., & Darimont, C. (2009) Planta
Med. 76, 566–571. doi:10.1055/s-0029-1240612
(266) Cheung, S., & Tai, J. (2007) Oncol Rep. 17(6):1525-31
(267) Scheckel, K.A., Degner, S.C., & Romagnolo, D.F. (2008)
J. Nutr. 138, 2098–2105. doi:10.3945/jn.108.090431
(268) Butt, M.S., Sultan, M.T., Butt, M.S., & Iqbal, J.
(2009) Crit. Rev. Food Sci. Nutr. 49, 538–551.
(269) Ban, J.O., Oh, J.H., Kim, T.M, Kim, D.J., Jeong, J.S.,
Han, S.B., & Hong, J.T. (2009) Arthritis Res. Ther. 11, R145.
(270) Keophiphath, M., Priem, F., Jacquemond-Collet, I.,
Clément, K., & Lacasa, D. (2009) J. Nutr. 139, 2055–2060.
(271) Salimzadeh, A., Alipoor, E., Dehghani, S., Yaseri, M.,
Hosseini, M., Feinle-Bisset, C., & Hosseinzadeh-Attar, M.J.
(2018) Int. J. Clin. Pract. 23, e13208. doi:10.1111/ijcp.13208
(272) Blumenthal, M., Busse, W., & Goldberg, A. (1998)
The Complete German Commission E Monographs:
Therapeutic Guide to Herbal Medicine, Integrative Medicine
Communications, Boston, MA
(273) Galeone, C., Tavani, A., Pelucchi, C., Negri, E., &
La Vecchia, C. (2009) Eur. J. Nutr. 48, 120–123. doi:10.1007/
(274) Kwak, J.S., Kim, J.Y., Paek, J.E., Lee, Y.J., Kim, H.R.,
Park, D.S., & Kwon, O. (2014) Nutr Res Pract. 8, 644–654.
(275) Budoff, M.J., Ahmadi, N., Gul, K.M., Liu, S.T., Flores, F.R.,
Tiano, J., Takasu, J., Miller, E., & Tsimikas, M. (2009) Prev.
Med. 49, 101–107. doi:10.1016/j.ypmed.2009.06.018
(276) Efendy, J.L., Simmons, D.L., Campbell, G.R., &
Campbell, J.H. (1997) Atherosclerosis 132, 37–42. doi:10.1016/
(277) Ferri, N., Yokoyama, K., Sadilek, M., Paoletti, R.,
Apitz-Castro, R., Gelb, M.H., & Corsini, A. (2003) Br. J.
Pharmacol. 138, 811–818. doi:10.1038/sj.bjp.0705126
(278) Durak, I., Oztürk, H.S., Olcay, E., & Güven, C. (2002) J. Herb.
Pharmacother. 2, 19–32
(279) Lau, B.H.S. (2006) J. Nutr. 136, 765S–768S. doi:10.1093/
(280) Lei, Y.P., Chen, H.W., Sheen, L.Y., & Lii, C.K. (2008) J. Nutr.
138, 996–1003. doi:10.1093/jn/138.6.996
(281) Gorinstein, S., Jastrzebski, Z., Namiesnik, J., Leontowicz, H., &
Trakhtenberg, S. (2007) Mol. Nutr. Food Res. 51, 1365–1381.
(282) Gonen, A., Harats, D., Rabinkov, A., Miron, T., Mirelman, D.,
Wilchek, M., Weiner, L., Ulman, E., Levkovitz, H.,
Ben-Shushan, D., & Shaish, A. (2005) Pathobiolog. 72,
325–334. doi:10.1159/000091330
(283) Koscielny, J., Klüssendorf, D., Latza, R., Schmitt, R.,
Radtke, H., Siegel, G., & Kiesewetter, H. (1999) Atherosclerosis
144, 237–249. doi:10.1016/S0021-9150(99)00060-X
(284) Williams, M.J., Sutherland, W.H., McCormick, M.P.,
Yeoman, D.J., & de Jong, S.A. (2005) Phytother. Res. 19,
314–319. doi:10.1002/ptr.1663
Jiang: Journal of aoaC international Vol. 102, no. 2, 2019 411
(314) Borek, C. (2006) J. Nutr. 136, 810S–812S. doi:10.1093/jn/136.3.810S
(315) Gupta, V.B., Indi, S.S., & Rao, K.S. (2009) Phytother. Res. 23,
111–115. doi:10.1002/ptr.2574
(316) Gupta, V.B., & Rao, K.S. (2007) Neurosci. Lett. 429, 75–80.
(317) Chauhan, N.B., & Sandoval, J. (2007) Phytother Res. 21,
629–640. doi:10.1002/ptr.2122
(318) Salman, H., Bergman, M., Bessler, H., Punsky, I., &
Djaldetti, M. (1999) Int. J. Immunopharmacol. 21, 589–597.
(319) Hassan, Z.M., Yaraee, R., Zare, N., Ghazanfari, T.,
Sarraf Nejad, A.H., & Nazori, B. (2003) Int. Immunopharmacol.
3, 1483–1489. doi:10.1016/S1567-5769(03)00161-9
(320) Chandrashekar, P.M., & Venkatesh, Y.P. (2009) J.
Ethnopharmacol. 124, 384–390. doi:10.1016/j.jep.2009.05.030
(321) Ishikawa, H., Saeki, T., Otani, T., Suzuki, T., Shimozuma, K.,
Nishino, H., Fakuda, S., & Morimoto, K. (2006) J. Nutr. 136,
816S–820S. doi:10.1093/jn/136.3.816S
(308) Thomson, M., Al-Qattan, K.K., Bordia, T., & Ali, M. (2006)
J. Nutr. 136, 800S–802S doi:10.1093/jn/136.3.800S
(309) Liu, C.T., Hse, H., Lii, C.K., Chen, P.S., & Sheen, L.Y.
(2005) Eur. J. Pharmacol. 516, 165–173. doi:10.1016/j.
(310) Sobenin, I.A., Nedosugova, L.V., Filatova, L.V.,
Balabolkin, M.I., Gorchakova, T.V., & Orekhov, A.N. (2008)
Acta Diabetol. 45, 1–6. doi:10.1007/s00592-007-0011-x
(311) Wang, J., Zhang, X., Lan, H., & Wang, W. (2017) Food Nutr.
Res. 61, 1377571. doi:10.1080/16546628.2017.1377571
(312) Aguilera, P., Chnez-Crdenas, M.E., Ortiz-Plata, A.,
Léon-Aparicio, D., Barrera, D., Espinoza-Rojo, M.,
Villeda-Hernndez, J., Snchez-García, A., &
Maldonado, P.D. (2010) Phytomedicine 17, 241–247.
(313) Saleem, S., Ahmad, M., Ahmad, A.S., Yousuf, S., Asari, M.A.,
Khan, M.B., Ishrat, T., & Islam, F. (2006) J. Med. Food. 9,
537–544. doi:10.1089/jmf.2006.9.537
... Among the variety of functional food materials, minor, but indispensable ingredients, such as herbs and spices, which are mostly used as flavoring additives and preservatives, contain an abundance of biofunctional molecules [2]. Most of these culinary herbs and spices, although primarily used in cooking, are also known for their nutraceutical values, as they have enormous health-promoting potentials [3]. ...
Full-text available
Mounting evidence support the potential benefits of functional foods or nutraceuticals for human health and diseases. Black cumin (Nigella sativa L.), a highly valued nutraceutical herb with a wide array of health benefits, has attracted growing interest from health-conscious individuals, the scientific community, and pharmaceutical industries. The pleiotropic pharmacological effects of black cumin, and its main bioactive component thymoquinone (TQ), have been manifested by their ability to attenuate oxidative stress and inflammation, and to promote immunity, cell survival, and energy metabolism, which underlie diverse health benefits, including protection against metabolic, cardiovascular, digestive, hepatic, renal, respiratory, reproductive, and neurological disorders, cancer, and so on. Furthermore, black cumin acts as an antidote, mitigating various toxicities and drug-induced side effects. Despite significant advances in pharmacological benefits, this miracle herb and its active components are still far from their clinical application. This review begins with highlighting the research trends in black cumin and revisiting phytochemical profiles. Subsequently, pharmacological attributes and health benefits of black cumin and TQ are critically reviewed. We overview molecular pharmacology to gain insight into the underlying mechanism of health benefits. Issues related to pharmacokinetic herb–drug interactions, drug delivery, and safety are also addressed. Identifying knowledge gaps, our current effort will direct future research to advance potential applications of black cumin and TQ in health and diseases.
... The exact mechanism of action of these phenol-compounds is not entirely understood. Still, it is known that they can be beneficial for human physiology and have been used in folk medicine since millennia [75]. They are currently being investigated for their anticancer activity [76][77][78]. ...
Full-text available
Natural compounds such as essential oils and tea have been used successfully in naturopathy and folk medicine for hundreds of years. Current research is unveiling the molecular role of their antibacterial, anti-inflammatory, and anticancer properties. Nevertheless, the effect of these compounds on bacteriophages is still poorly understood. The application of bacteriophages against bacteria has gained a particular interest in recent years due to, e.g., the constant rise of antimicrobial resistance to antibiotics, or an increasing awareness of different types of microbiota and their potential contribution to gastrointestinal diseases, including inflammatory and malignant conditions. Thus, a better knowledge of how dietary products can affect bacteriophages and, in turn, the whole gut microbiome can help maintain healthy homeostasis, reducing the risk of developing diseases such as diverse types of gastroenteritis, inflammatory bowel disease, or even cancer. The present review summarizes the effect of dietary compounds on the physiology of bacteriophages. In a majority of works, the substance class of polyphenols showed a particular activity against bacteriophages, and the primary mechanism of action involved structural damage of the capsid, inhibiting bacteriophage activity and infectivity. Some further dietary compounds such as caffeine, salt or oregano have been shown to induce or suppress prophages, whereas others, such as the natural sweeter stevia, promoted species-specific phage responses. A better understanding of how dietary compounds could selectively, and specifically, modulate the activity of individual phages opens the possibility to reorganize the microbial network as an additional strategy to support in the combat, or in prevention, of gastrointestinal diseases, including inflammation and cancer.
... Herbs and spices grown in the mountainous and coastal regions in the Mediterranean area are a key ingredient in the unique flavor of many Mediterranean dishes, while many herbs and spices have been shown to extend potential health benefits [64]. Including but not limited to cumin, parsley, oregano, rosemary, thyme, and sage, herbs and spices are crucial to the unique flavor profile of the MD [65]. ...
Full-text available
The Mediterranean diet is a food pattern incorporated into a set of lifestyle practices typical of Greece and Southern Italy in the early 1960s, where adult life expectancy was notably high, while rates of diet-related chronic diseases were low. The Mediterranean diet was described initially by the work of LG Allbaugh, commissioned by the Rockefeller foundation and the Greek government post-WW2 on the Greek island of Crete in 1948. The Mediterranean diet was accepted as Intangible Cultural Heritage of Humanity by UNESCO in 2013. The primary advantages of the Mediterranean diet include health benefits pertinent to cardiovascular, metabolic syndrome, and cognition.
... Inflammation is also managed using medicinal plants such as Azima tetracantha (Lam) 5 , Eugenia jambolana 6 among others. Herbal medicines serve as better al-ternatives for they are arguably readily available, cheap and possess fewer side effects hence the need to search for new bioactive compounds in medicinal plants 7 . E. globulus is an evergreen tree with a straight trunk of about 0.6 to 2 meters in diameter and a height of 40-70 meters tall. ...
Full-text available
Background: Inflammation is an immune response characterized by swelling, redness, pain and heat. Inflammation is main- ly managed using conventional medicines that are associated with many side effects. Plant-based remedies are considerably better alternative therapies for they have fewer side effects. Objective: This study aimed at determining the anti-inflammatory potential of dichloromethane (DCM) leaf extracts of Eucalyptus globulus and Senna didymobotrya in mice. Methods: Fresh leaves of these plants were harvested from Embu County, Kenya. Quantitative phytochemical analysis was done using Gas Chromatography-Mass Spectrometry (GC-MS). Anti-inflammatory test comprised nine groups of five animals each: normal, negative, positive controls and 6 experimental groups. Inflammation was induced with Carrageenan. One hour post-treatment, the different groups were intraperitoneally administered with the reference drug, diclofenac, 3% DMSO and six DCM leaf extracts at doses of 25, 50, 100, 150, 200 and 250mg/kgbw. Results: GC-MS results revealed α-phellandrene, camphene, terpinolene, and limonene among others. Anti-inflammatory effects showed that extract doses of 100,150,200 and 250mg/kg bw significantly reduced the inflamed paw. Doses of 200 and 250mg/kgbw in both plants were more potent and compared with diclofenac. E. globulus extract dose of 250mg kg bw reduced inflamed paw in the 1st , 2nd, 3rd and 4th hours, by 2.27,6.52,9.09 and 10.90% respectively while S.didymobotrya at similar dose ranges, inflamed paw reduced by 2.41, 5.43, 8.31 and 9.05% respectively. Conclusion: E. globulus and S. didymobotrya have potent anti-inflammatory activities, attributed to their constituent phyto- chemicals. This study confirms the traditional use of these plants in treating inflammation. Keywords: Eucalyptus globulus; Senna didymobtrya; inflammation; phytochemicals.
... Moreover, spices and herbs are an exceptionally rich source of nutritionally important phenolic compounds [3]. These phenolic compounds are primarily responsible for the potent antioxidative, digestive stimulative, hypolipidemic, antibacterial, anti-inflammatory, antiviral, and anticancer properties of spices and herbs [4][5][6]. ...
Full-text available
Spices and herbs are well-known for being rich in healthy bioactive metabolites. In recent years, interest in the fatty acid composition of different foods has greatly increased. Thus, the present study was designed to characterize the fatty acid composition of 34 widely used spices and herbs. Utilizing gas chromatography (GC) flame ionization detection (FID) and GC mass spectrom-etry (MS), we identified and quantified 18 fatty acids. This showed a significant variation among the studied spices and herbs. In general, oleic and linoleic acid dominate in seed spices, whereas palmitic, stearic, oleic, linoleic, and α-linolenic acids are the major constituents of herbs. Among the studied spices and herbs, the ratio of n−6/n−3 polyunsaturated fatty acids (PUFAs) was recorded to be in the range of 0.36 (oregano) to 85.99 (cumin), whereas the ratio of PUFAs/saturated fatty acids (SFAs) ranged from 0.17 (nutmeg) to 4.90 (cumin). Cumin, coriander, fennel, and dill seeds represent the healthiest fatty acid profile, based upon fat quality indices such as the ratio of hypocholes-terolemic/hypercholesterolemic (h/H) fatty acids, the atherogenic index (AI), and the thrombogenic index (TI). All these seed spices belong to the Apiaceae family of plants, which are an exceptionally rich source of monounsaturated fatty acids (MUFAs) in the form of petroselinic acid (C18:1n12), with a very small amount of SFAs.
... Since time immemorial several traditional medicines worldwide have been using a combination of ingredients including spices. 1 The chemical constituents and spices having significant biological properties including antimicrobial, antioxidant, anti-inflammatory, anti-cancerous were well documented in various scientific reports. 2,3 These spices have the potential to be used ass preservatives in many processed due to its antimicrobial and antioxidant properties. ...
Full-text available
Herbs and spices are the very best way to add flavor and dimension to a dish without adding fat, salt or calories. In fact, some herbs and spices already include a little something extra, like antioxidants. Antioxidants are substances that slow or prevent the oxidative process in which cells are damaged by free radicals, which can lead to cell dysfunction. These powerful nutrients have been linked to the prevention of heart disease and diabetes, improving immune function and lowering the risk of infection and even some cancers. The bioactive compounds present in spices having antioxidant properties mainly consists of flavonoids, phenolic compounds, sulfur-containing compounds, tannins, alkaloids, phenolic diterpenes, and vitamins. While we hear a lot about the antioxidants found in dark chocolate and red wine, spices like ground cloves, oregano leaves, ginger, cinnamon, turmeric and yellow mustard seed are the real antioxidant stars – delivering a higher concentration of antioxidants per 100g than dark chocolate, wine, even blueberries and whole grain cereal. Plus, they have none of the calories found in chocolate or the drawbacks associated with alcohol consumption.
Herbs and spices are recommended to increase flavor and displace salt in the diet. Accumulating evidence suggests herbs and spices may improve risk factors for cardiometabolic diseases. In this narrative review, an overview of evidence from human clinical trials examining the effect of herbs and spices on risk factors for cardiometabolic diseases is provided. Human clinical trials examining supplemental doses of individual spices and herbs, or the active compounds, have yielded some evidence showing improvements to lipid and lipoprotein levels, glycemic control, blood pressure, adiposity, inflammation, and oxidative stress. However, cautious interpretation is warranted because of methodological limitations and substantial between-trial heterogeneity in the findings. Evidence from acute studies suggests intake of mixed herbs and spices as part of a high-saturated fat, high-carbohydrate meal reduces postprandial metabolic impairments, including lipemia, oxidative stress, and endothelial dysfunction. Limited studies have examined the postprandial metabolic effects of incorporating mixed herbs and spices into healthy meals, and, to our knowledge, no trials have assessed the effect of longer-term intake of mixed herbs and spices on risk factors for cardiometabolic diseases. To inform evidence-based guidelines for intake of herbs and spices for general health and cardiometabolic disease risk reduction, rigorously conducted randomized controlled trials are needed, particularly trials examining herb and spice doses that can be incorporated into healthy dietary patterns.
The aflatoxin contamination of chilli pepper grown and marketed in Tamil Nadu, a southern Indian state was assessed. Chilli samples were collected at different stages of the value chain and were quantified using the enzyme‐linked immunosorbent assay (ELISA) test. Forty‐two representative samples were collected from four districts identified as the hub for production, distribution, agro‐processing industries, and retail stores. In addition, interviews were conducted amongst the chilli farmers, vendors, and agro‐industrialists across the hubs to assess their knowledge on aflatoxin contamination and safe handling practices. The maximum aflatoxin content determined in the chilli pepper was 37.8 µg/kg. Almost 66.7% of samples collected from the retail outlets had aflatoxin values above 10 µg/kg. The total aflatoxin content in the samples collected across the value chain was in the range of 3.83 to 37.80 µg/kg. Statistical analysis on aflatoxin contents showed that there were significant differences (p<0.05) between the districts representing different operations of value‐chain. The detected aflatoxin content was highest in samples collected from Dindigul district and least in Erode district. The results of the perception study showed that respondents into farming and trade activities had very little or no knowledge of aflatoxin contamination of chilli. The prevalence of unacceptable levels of aflatoxin in the chilli supply chain in the districts studied is probably due to tropical climatic conditions and poor handling practices of chilli.
Peppers are consumed all over the world, have several benefits to human health, such as antioxidant properties that can prevent diseases related to free radicals such as cardiovascular, inflammatory diseases, cancer, among others. This work aimed to evaluate the antioxidant capacity (AOC) of 36 varieties of peppers through ABTS and DPPH radical scavenging, electroanalytical assays, and to verify the vasorelaxant properties of selected samples. The greater the amount of capsaicin found in the extracts, the higher the AOC the greater the vasorelaxation. Naga had the highest scoring for antioxidant capacity, pout showed the lowest antioxidant capacity, vase pyramid intermediate level, whereas the capsaicin content followed the same trend. Extracts from all pepper varieties studied presented vasorelaxant properties in independent and dependent endothelial pathways.
This systematic review and meta-analysis examined the association between spicy food (chilli pepper, chilli sauce, or chilli oil) consumption with cardiovascular and all-cause mortality. Medline and EMBASE were searched from their inception until February 2020 to identify relevant prospective cohort studies. Hazard ratios (HRs)/relative risk (RRs) were pooled via random-effect meta-analysis. Of the 4387 citations identified, 4 studies (from the United States, China, Italy, and Iran) were included in the meta-analysis. The included studies involved a total of 564 748 adults (aged ≥18 years; 51.2% female) followed over a median duration of 9.7 years. The pooled data suggested that compared with people who did not regularly consume spicy food (none/<1 d/wk), regular consumers of spicy food experienced a 12% (HR/RR pooled 0.88, 95% CI, 0.86-0.90; I ² = 0%) lower risk of all-cause mortality. Moreover, spicy food consumption was associated with significant reduction in the risk of death from cardiac diseases (HR/RR pooled 0.82, 0.73-0.91; I ² = 0%), but not from cerebrovascular disorders (HR/RR pooled 0.79, 0.53-1.17; I ² = 72.2%). In conclusion, available epidemiological studies suggest that the consumption of spicy chilli food is associated with reduced risk of all-cause as well as heart disease–related mortality. Further studies in different populations are needed to confirm this association.
Full-text available
Rosmarinus officinalis L. (Lamiaceae), popularly known as rosemary, is used for food flavoring, and in folk medicine, as an antispasmodic, analgesic, anti-rheumatic, diuretic, and antiepileptic agent. Rosemary is an herb widely used in folk medicine, cosmetics, and phytotherapy and for flavoring of food products. Studies have focused on various biological activities of the secondary metabolites of this plant, such as rosmarinic acid, which have powerful antioxidant, hepato-protective, antimicrobial, anti-nociceptive, and anti-inflammatory properties.
Full-text available
In this study, the aim was to determine the bioaccessibilities of carnosic acid in sage and rosemary and in vitro inhibitory effects of these samples on lipid and starch digestive enzymes by evaluating the lipase, α-amylase and α-glucosidase enzyme inhibition activities. The content of carnosic acid in rosemary (18.72 ± 0.33 mg/g) was found to be higher than that content of that in sage (3.76 ± 0.13 mg/g) (p < 0.05). The carnosic acid bioaccessibilities were found as 45.10 ± 1.88% and 38.32 ± 0.21% in sage and rosemary, respectively. The tested sage and rosemary showed inhibitory activity against α-glucosidase (Concentration of inhibitor required to produce a 50% inhibition of the initial rate of reaction - IC50 88.49 ± 2.35, 76.80 ± 1.68 μg/mL, respectively), α-amylase (IC50 107.65 ± 12.64, 95.65 ± 2.73 μg/mL, respectively) and lipase (IC50 6.20 ± 0.63, 4.31 ± 0.62 μg/mL, respectively). Furthermore, to the best of our knowledge, this is the first work that carnosic acid standard equivalent inhibition capacities (CAEIC50) for these food samples were determined and these values were in agreement with the IC50 values. These results show that sage and rosemary are potent inhibitors of lipase, α-amylase and α-glucosidase digestive enzymes.
Full-text available
Pleiotropic effects of spices on health, particularly on glucose metabolism and energy regulation, deserve further clinical investigation into their efficacy.
Full-text available
Background Postoperative nausea and vomiting (PONV) are among the most frequent complications following laparoscopic cholecystectomy. Recently, some studies have shown ginger, as an herbal medicine, to be effective and safe in PONV prevention; however, there is no evidence of its efficacy in the Iranian population. Objective The aim of this study was to determine the effect of oral ginger on PONV prevention after laparoscopic cholecystectomy. Methods This double-blind, randomized, placebo-controlled clinical trial was performed on women who were undergoing laparoscopic cholecystectomy in Imam Raza Hospital, Mashhad, Iran between April and November, 2016. Patients were divided randomly into two groups of G) intervention group (n=75, received 2 capsules containing 250 mg ginger) and P) placebo group (n=75, received 2 placebo capsules) one hour before surgery. Nausea severity and vomiting frequency were evaluated at 2, 4, 6, and 12 hours after the operation. Data analysis was done by SPSS version 16.0 software with Chi-square test, Independent-sample-t-test, repeated measure ANOVA and Mann–Whitney U test. Results The two groups were homogenous in terms of age, gender and surgery duration. The severity of nausea was lower in the ginger group at the 2, 4, 6, and 12 hours after the operation; however, these differences were statically significant only at 2 (p=0.034) and 12 hours (p=0.043). Although the incidence of vomiting was higher in the placebo group in the 2nd and 12th hours after surgery, the number of vomiting episodes in 2, 4, 6 and 12 hours after surgery was statistically similar in the two groups (p>0.05). The nausea severity was significantly changed during 12 hours of study in both groups (p=0.001), however the nausea severity was always lower in the ginger group (p=0.078). Conclusion This study demonstrated that 500mg oral ginger one hour before surgery in women who were undergoing laparoscopic cholecystectomy is effective in decreasing severity of PONV. Trial registration The trial was registered at the Iranian Registry of Clinical Trials ( with the Irct ID: IRCT2016122222218N2. Funding The study was financially supported by Deputy of Research of Mashhad University of Medical Sciences.
Full-text available
The cornerstone of initial management for hypertriglyceridemia (HTG) is lifestyle modification. The combination of weight loss through caloric restriction, alteration in macronutrient composition and increased energy expenditure reduces TG levels by approximately 50%. The addition of cinnamon, cacao products and isocaloric substitution of 1 serving of nuts may contribute another 5-15% lowering of TG. This can be particularly beneficial in patients with HTG who are at increased risk of cardiovascular disease.