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Investigation of the effect of ginger on the lipid levels: A double blind controlled clinical trial

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Abstract

To study the effect of fine powder of ginger on lipid level in volunteer patients. This is a double blind controlled clinical trial study in 2 cardiac clinics Cardiac Disease Clinic, Babol, north of Iran, between April to May 2004. We randomly divided the patients with hyperlipidemia into 2 groups, treatment group (receiving ginger capsules 3 g/day in 3 divided doses) and placebo group (lactose capsule 3 g/day in 3 divided doses) for 45 days. All subjects with diabetes mellitus, hypothyroidism, nephrotic syndrome, and alcohol drinking, pregnancy and peptic ulcer were excluded. Lipid concentrations profile before and after treatment was measured by enzymatic assay. Forty-five patients in the treatment group and 40 patients in placebo group participated in this study. There was a significant reduce in triglyceride, cholesterol, low density lipoprotein (LDL), very low density lipoprotein (VLDL), levels of before and after study separately in each group (p<0.05). Mean changes in triglyceride and cholesterol levels of ginger group were significantly higher than placebo group (p<0.05). Mean reduction in LDL level and increase in high density lipoprotein level of ginger group were higher than the placebo group, but in VLDL level of placebo was higher than ginger (p>0.05). The results show that ginger has a significant lipid lowering effect compared to placebo.
Investigation of the effect of ginger on the lipid levels, a
double blind controlled clinical trial
Reza Alizadeh-Navaei, MD, Fatemeh Roozbeh, MD, Mehrdad Saravi, MD,
Mehdi Pouramir, PhD, Farzad Jalali, MD, Ali A. Moghadamnia, PhD.
179
ABSTRACT


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20052004

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3g
3g
45



   45      
40
      
LDL
VLDL

p
0.05


p
0.05
   LDL   
   HDL   
 VLDL     

p
0.05


Objective: To study the effect of fine powder of ginger
on lipid level in volunteer patients.
Method: is is a double blind controlled clinical
trial study in 2 cardiac clinics Cardiac Disease Clinic,
Babol, north of Iran, between April to May 2004. We
randomly divided the patients with hyperlipidemia
into 2 groups, treatment group (receiving ginger
capsules 3 g/day in 3 divided doses)
Original Articles
and placebo group (lactose capsule 3 g/day in 3
divided doses) for 45 days. All subjects with diabetes
mellitus, hypothyroidism, nephrotic syndrome, and
alcohol drinking, pregnancy and peptic ulcer were
excluded. Lipid concentrations profile before and
after treatment was measured by enzymatic assay.
Results: Forty-five patients in the treatment group
and 40 patients in placebo group participated in this
study. ere was a significant reduce in triglyceride,
cholesterol, low density lipoprotein (LDL), very low
density lipoprotein (VLDL), levels of before and
after study separately in each group (p<0.05). Mean
changes in triglyceride and cholesterol levels of ginger
group were significantly higher than placebo group
(p<0.05). Mean reduction in LDL level and increase
in high density lipoprotein level of ginger group were
higher than the placebo group, but in VLDL level of
placebo was higher than ginger (p>0.05).
Conclusion: e results show that ginger has a
significant lipid lowering effect compared to placebo.
Saudi Med J 2008; Vol. 29 (9):
From the Departments of Pharmacology (Navaei, Roozbeh,
Moghadamnia), Internal Medicine (Saravi, Jalali), and Biochemistry
(Amir), Babol University of Medical Sciences, Babol, Iran.
Received 31st May 2008. Accepted 18th August 2008.
Address correspondence and reprint request to: Dr. Reza A. Navaei,
Department of Pharmacology, Babol University of Medical Sciences,
Babol, Iran. Tel. +98 11114756. Fax. +98 111-2294718.
E-mail: reza_nava@yahoo.com
Hyperlipidemia mirrors the onset of abnormality of
lipid metabolism secondary to the manifestation
and progression of the atherosclerotic disease. In addition
to diet, the use of herbal medicine as a pharmacologic
modality in preventing alteration in lipid metabolism has
received a wide attention from several workers.1 Ginger
(Zingiber officinale, Zingiberaceae), a well-known
spice plant, sweet, pungent, heating appetizer has been
used in traditional oriental medicines for long time. Its
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Investigation of the effect of ginger on the lipid levels … Alizadeh-Navaei et al
Saudi Med J 2008; Vol. 29 (9) www.smj.org.sa
extract and major pungent principles have been shown
to exhibit a variety of biological activities.2,3 It has been
used to treat a number of medical conditions, including
headache, colds, and arthritis.4 Ginger reduces symptoms
in patients with nausea of pregnancy, motion sickness,
and postoperative nausea and vomiting.5-8 Limited in
vitro studies have shown that water and organic solvent
extracts of ginger possess antioxidant active component
in ginger properties.9-11 e main antioxidant active
materials in ginger are the gingerols and shogaols and
some related phenolic ketone derivatives.12 Ginger acts
as a hypolipidemic agents in cholesterol-fed rabbits.13
Ginger has been shown that can significantly reduce
serum total cholesterol and triglyceride and increase
the high density lipoprotein (HDL) cholesterol
level as compared to pathogenic diabetic rats.13 A
combination of ginger and garlic has been reported to
have hypoglycemic and hypolipidemic effects in albino
rats.14 Etanolic ginger extract consumption has also been
shown to reduce plasma cholesterol and inhibit low
density lipoprotein (LDL) oxidation in atherosclerotic,
a-lipoprotein E-deficient mice.15 It has been suggested
that the aqueous extract of ginger might inhibit the
intestinal absorption of dietary fat by inhibiting its
hydrolysis.16 On the other hand, one clinical study
shows that ginger could not affect the blood lipid and
sugar level,17 but there are no adequate findings of
clinical study of lipid lowering effect of ginger. Evidence
continues to accumulate from epidemiological studies
that elevated plasma concentrations of lipoprotein (a)
[LP (a)] are a risk factor for a variety of atherosclerotic
and thrombotic disorders.18 High plasma levels of LP (a)
are strongly associated with coronary artery disease, and
LP(a) has been established as an independent risk factor
and marker for atherosclerosis.19 On the other hand,
hyperhomocysteinemia is a risk factor for cardiovascular
disease.20 Plasma homocysteine predicts progression of
atherosclerosis.21 On the basis of this, in the present
study we have investigated the effect of ginger on blood
lipids and LP (a) and homocysteine in a double blind,
placebo-control trail study.
Methods. is study was a randomized, double
blind, placebo control trial performed between April
2004 and May 2005. All patients with hyperlipidemia
that returned to 2 cardiac clinic in Babol (Iran) who had
fasting triglyceride of >200 mg/dl or cholesterol >200
mg/dl were enrolled in this trial. Forty-five patients
with hyperlipidemia in treatment group and 40 patients
with hyperlipidemia in placebo group participated in
this study. Exclusions criteria were diabetes mellitus,
hypothyroidism, and nephrotic syndrome, alcohol
drinking, pregnancy and peptic ulcer. We obtained
written informed consent from all the subjects before
the study period. Ethics committee of Babol University
of Medical Sciences approved the study. Patients were
randomized to receive ginger capsules (3 g/day in 3
divided dose) or lactose capsule (3 g/day in 3 divided
dose) for 45 days. e dried rhizome of ginger was
purchased from a valid market (Rezaeian, Tehran,
Iran) and powdered as a fine particle. e fine powder
was handed to a pharmaceutical Lab (Tehran, Iran)
to prepare the capsules containing 500 mg ginger in
each. Lactose (Merck, Germany) was used to prepare
the placebo. Ginger (or placebo) capsules were given
to all patients in one package including 6 bottles of
drugs or placebo. Blood sample (5 ml) was taken before
and after treatment and fasting serum triglyceride,
cholesterol, HDL, LDL, and VLDL were measured by
enzymatic assay and lipoprotein-a and homocysteine
levels were measured using electro immunoassay and
Enzyme-Linked Immuno-Sorbent Assay.
Statistical analysis was carried out using the
Statistical Package for Social Sciences Version 10.5
software. Variations of lipids level were analyzed using
paired sample student t-test. e differences between
the groups were compared by unpaired sample student
t-test, and Mann-Whitney U test and gender distribution
between the 2 groups was analyzed using Fishers exact
test. Probability values of less than 0.05 were considered
statistically significant.
Result. e mean ±SD age of patients in the treatment
group was 53.8±11.8 years, and the control group was
53.5±11 years (p=0.905). e mean ±SD body mass
index of patients in the treatment groups was 31±4.4
kg/m2 and in the control group was 34.5±7.7 kg/m2
(p=0.83). ere were 16 (35.6%) males and 29 (64.4)
females in the treatment group and 18 (45%) males and
22 (55%) females in the control group (p=0.387). Tables
1 and 2 show the effects of administration of the ginger
on the levels of lipid lipoprotein-a and homocysteine.
Table 1 demonstrates the serum lipid profile of ginger
and placebo group at the beginning and at the end
of the trial. Within the group analysis, the levels of
triglyceride, cholesterol, LDL, VLDL, Lipoprotein-a
and homocysteine were decreased in both groups at the
end of the trial (p<0.05). e level of HDL increased
in response to ginger (p<0.05) but not in the placebo
group. ere was a significant difference between
the level of cholesterol and triglyceride in the ginger
group compared to placebo (p<0.05). Some alterations
were seen between the level of other parameters.
Also, HDL was increased in the ginger group, but no
significant differences were seen. However, the levels
of LDL decreased, but the difference was not statistical
significant. e dose of ginger (3 g/daily) had no effect
on the concentration of VLDL, lipoprotein-a and
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Investigation of the effect of ginger on the lipid levels … Alizadeh-Navaei et al
homocysteine. Non-significant reduction in LDL was
observed when ginger was administered at 3 g/daily for
45 days. e changes in the ginger treatment compared
to the changes in placebo group are presented in Table 2.
e mean changes in triglyceride and cholesterol levels
of ginger receiving subjects were higher than placebo
(p<0.05) (Table 2). ere was no significant change in
the ginger treatment group compared to placebo for
lipoprotein-a and homocysteine.
Discussion. According to the result, there was a
significant decrease of level of triglyceride and cholesterol
after administration of ginger in comparison with placebo
(p<0.05). ese data were consistent with the previous
studies.17,22 Some investigations have been reported
a decrease in levels of cholesterol and triglycerides in
the serum of rats receiving oral and intraperitoneal
administration of ginger.23 ere was a significant
reduction in level of cholesterol was observed in the rats
given a high dose of ginger (500 mg/kg) either orally
or intraperitoneal. No significant change in triglyceride
was observed in the serum of rats receiving either oral or
intraperitoneal ginger. e anti-hypercholesterolemic
effect of ginger was previously shown in rats fed with a
high-cholesterol diet for 24 days.24 ese workers also
reported that there was no immediate effect of ginger on
serum cholesterol. is confirms our finding that ginger
given daily for a period of 12 weeks orally significantly
reduced the serum cholesterol in the patients (Table 2).
e hypocholesterolemic effect of ginger could have
possibly resulted, at least in part, from the inhibition
of cellular cholesterol biosynthesis observed after
consumption of ginger extract.15 Reduced cellular
cholesterol biosynthesis is associated with increased
activity of the LDL receptor, which in turn leads to
enhanced removal of LDL from plasma, resulting in
reduced plasma cholesterol concentration.25 ese
results are in agreement with previously reported data,
showing that plant foods possess cholesterol-suppressive
capacity.26 It has been previously reported that the plant
food-derived ingredients, ß-carotene and lycopene, also
act as hypocholesterolemic agents, secondary to their
inhibitory effect on cellular cholesterol biosynthesis.27
It has been reported that consumption of 250 mg/day
of ginger extract for 10 weeks resulted in reduction
of triglyceride level in mice.27 On the other hand,
ethanolic extract of ginger (200 mg/kg for 10 weeks)
shows reduce serum triglyceride levels in cholesterol
fed rabbits compared with gemfibrozil.1 Lipid lowering
effect of ginger is possible that ginger decreased lipid by
increasing pancreatic lipase and amylase,24,28 inhibit lipid
hydrolyze in intestinal tract16 reducing lipid peroxidase29
increasing intestinal peristaltism,30 increasing cholesterol
conversion to bile acids.31 Feeding rats ginger significantly
elevated the activity of hepatic cholesterol-7-hydroxylase,
the rate-limiting enzyme in bile acids biosynthesis,
thereby stimulating cholesterol conversion to bile acids,
resulting in elimination of cholesterol from the body.31
In addition, a pure constituent from ginger [E-8 beta,
17 epoxylabd-12-ene-15, 16-dial (ZT)], was shown to
inhibit cholesterol biosynthesis in homogenated rat
liver.32 However, Verma et al reported that air dried
ginger powder (0.1 g/kg per os for 75 days) did not
lower blood lipids to any significant extent in rabbits by
cholesterol feeding (0.3 gr/kg per os).33 In another study,
Table 1 - Fasting lipid, lipoprotein-a and homocysteine levels (Mean ±SEM) before and after treatment (mg/dl).
Variable Ginger Placebo
Before After P-value* Before After P-value*
Triglyceride 320.2 ± 13.1 284 ± 11.5 0.000 331.4 ± 17.1 304.7 ± 15 0.004
Cholesterol 269 ± 4.9 241.5 ± 7.5 0.000 263.8 ± 5 249.2 ± 4.9 0.001
HDL 39.8 ± 0.7 42.6 ± 0.8 0.002 41.5 ± 1.3 41.3 ± 1 0.845
LDL 168.5 ± 5.4 151.2 ± 4.9 0.000 162.6 ± 5.3 152.7 ± 4.5 0.005
VLDL 28.9 ± 1.3 25.6 ± 0.9 0.001 31.5 ± 2.3 27.4 ± 1.4 0.008
Lipoprotein-a 23.1 ± 2 19.3 ± 1.6 0.000 29.6 ± 1.4 24.3 ± 3 0.009
homocysteine 10.7 ± 0.5 9.5 ± 0.4 0.012 10.8 ± 0.9 9.3 ± 0.5 0.012
* Paired t-test, HDL - high density lipoprotein, LDL - low density lipoprotein, VDL- very low density lipoprotein
Table 2 - Mean (±SEM) differences (mg/dl) lipids, lipoprotein-a and
homocysteine between groups before and after treatment.
Variable Ginger Placebo P-value
Triglyceride 36.2 ± 7.7 26.7 ± 8.6 0.039*
Cholesterol 27.5 ± 5.6 14.5 ± 4 0.027*
HDL 1.8 ± 0.5 0.17 ± 0.8 0.058†
LDL 17.3 ± 2.9 9.9 ± 3.3 0.093†
VLDL 3.3 ± 0.9 4 ± 1.3 0.638†
Lipoprotein-a 3.8 ± 0.9 5.2 ± 1.7 0.451†
Homocysteine 1.2 ± 0.4 1.5 ± 0.5 0.638†
* T-test, †Mann-Whitney, HDL - high density lipoprotein, LDL -low
density lipoprotein, VLDL - very low density lipoprotein
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Saudi Med J 2008; Vol. 29 (9) www.smj.org.sa
patients with coronary artery disease, ginger failed to
lower blood lipids when it was given in powdered form
(4 g) daily for a period of 3 months.31 In the present
study, significant difference (p<0.05) in HDL response
before and after ginger was considered after 45 days of
daily intake of 3000 mg of ginger powder but there was
no significant difference in placebo group. Bhandari
et al13 reported that the ethanolic extract of Zingiber
officinale (200 mg/kg for 20 days) significantly increased
the HDL-cholesterol level. Fuhrman et al15 showed that
consumption of 250 mg/kg of ginger extract resulted in
reductions in LDL of apolipoprotein E-deficient mice.15
Ginger extract consumption can result in accumulation
of active ingredients within the cells, as well as in the
cell plasma membrane, thus affecting cellular enzymes,
and plasma membrane receptors. It has been shown that
ginger extract consumption reduces the cellular uptake
of oxidized LDL, possibly due to steric modification of
plasma lipoprotein receptors.15 We have observed no
significant reduction in serum LDL levels in present
study. However, the result of our study, regarding LDL
level was not consistent with the previous study.15 It may
be due to the level of given dose of ginger to our patients.
Since the equivalent dose of ginger extract with powder
that was used in this study was 90 mg crude extract
of ginger daily. at is in contrary with the previous
study.15 It was suggested that the study to be continue
with different doses or different procedures. In this
study, the finding of a non-significant HDL lowering
effect lends itself to several possible interpretations; it
is possible that ginger powder has no effect on LDL.
e limitation of this study was having a single center
and multicenter study with larger patients should be
conducted.
In conclusion, the significant reduction in serum
cholesterol by ginger could possibly play an important
in the prevention and development of atherosclerosis.
e unique ability of ginger to lower serum cholesterol
and triglyceride levels is clinically important, because
its daily intake for a prolonged period will neither lead
to side-effects nor to complications as normally occurs
with anti-hyperlipidemic drugs.
Acknowledgment. e authors would like to thank the Babol
University of Medical Sciences for financial support of this study and
the laboratory technicians for their collaboration in measurement of the
samples.
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... Therapeutic properties of O. sanctum, Zingiber officinale Rose (Zingiberaceae), and Piper nigrum Linn (Piperaceae) are widely reported and major components of these three herbs are well characterized and are also used in immune and inflammatory conditions such as diabetes, obesity, asthma (Damanhouri and Ahmad 2014;de Lima et al. 2018;Singh and Chaudhuri 2018). The plethora of scientific literature and classical Ayurvedic text suggests that the herbs O. sanctum, Z. officinale, and P. nigrum have a wide variety of proven functions and specific properties such as immunomodulatory, anti-inflammatory, and ability to increase the bioavailability of active compounds, respectively (Alizadeh-Navaei et al. 2008;Damanhouri and Ahmad 2014;Parasuraman et al. 2015). It is noteworthy to mention that these herbal extracts possess a vast number of 'phytochemical constituents' whose bioactivities were assigned to such active principal ingredients (APIs). ...
... In the recent past, the in vivo studies conducted with extracts of O. sanctum, Z. officinale, and P. nigrum reported no changes in hematological profile of healthy animals even upon prolonged administration (Rong et al. 2009;Sriwiriyajan et al. 2016;Singh and Chaudhuri 2018). However, O. sanctum, Z. officinale, and P. nigrum extracts were known to regulate the lipid metabolism, insulin resistance and inflammatory markers specially C-Reactive Protein (CRP), LPS and IL-6 levels (Alizadeh-Navaei et al. 2008;Damanhouri and Ahmad 2014;Parasuraman et al. 2015). ...
... This finding was corroborated with a study conducted in normal albino rabbits fed on diet mixed with fresh leaves of O. sanctum (1-2 g/100 g of diet/ 4 weeks) resulted in significant lowering of plasma phospholipid, TG, total and LDL-cholesterol levels, with significant increase in HDL-cholesterol (Sarkar et al. 1994). Interestingly many studies have shown favourable regulation of lipid profile along with anti-diabetic and anti-hyperlipidemic activities with these three selected herbal extracts (Alizadeh-Navaei et al. 2008;Damanhouri and Ahmad 2014;Parasuraman et al. 2015;Sarfaraz et al. 2016). These findings clearly suggest that herbal extracts of present study have immense prebiotic potential, apart from regulating the intestinal bacteria, thereby improving the health status. ...
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... Many recent studies have demonstrated blood-lowering effects of ginger supplementation in humans. A significant reduction in serum/cholesterol levels was reported in hyperlipidemic patients who were given ginger supplement at a dose of 3 g/day for 45 days in one study and for 4 weeks in another study [113,114]. ...
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... Whilst another showed that a 2 g ginger treatment significantly reduced TG levels in the blood compared to the placebo group in obese women [84]. Moreover, a randomized double blinded study examined the effects of 3 g of ginger powder for 45 days on CVD patients in Iran, concluding that ginger powder caused a significant reduction in TGs, cholesterol, LDL, and very low-density lipoprotein (VLDL) levels in the blood [88]. ...
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Medicinal plants have been the keystone of health care since ancient time. Their innumerable uses have been documented and transformed through the generation for over more than 4000 years. In the early 19th century, as soon as the scientific investigations began, numerous plant based drugs have been made available to cure large number of global diseases. The 21st century started with exploration of these traditional remedies to meet patient needs. Now we are in the era where science and technologies have evolved to elucidate the safety and efficacy of traditional medicines. Even though much more information on uses of plant/plant parts in various health practices is still unrecorded. This book will present an overall illustration of some selected medicinal plants and their medico biological application. It will also throw light on critical areas of ongoing research, transforming the information on medicinal plants and their recent applications.
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Chapter
Ginger (Zingiber officinale) is well known for its anti-nausea and anti-inflammatory effects. It has been shown to have several gastrointestinal benefits in clinical research, as it improves digestion by stimulating salivary flow, gastric motility, gastric acid production, bile flow, and gall bladder kinesis. It may be beneficial for gingivitis, coronary artery disease, hyperlipidemia, nausea and vomiting of pregnancy, motion sickness, post-operative nausea, chemotherapy-induced nausea, gastroparesis, dysmenorrhea, menorrhagia, menopause, male infertility, osteoarthritis, muscle pain, migraine headache, and colorectal cancer prevention. In addition, ginger or its constituents have antiplatelet and antioxidant activity. This chapter examines some of the scientific research conducted on ginger, both alone and in combination formulas, for treating numerous health conditions. It summarizes results from several human studies of the ginger’s use in treating oral and dental, cardiometabolic, gastrointestinal, urogenital, neurological, and oncologic disorders. Finally, the chapter presents a list of ginger’s active constituents, different Commonly Used Preparations and Dosage, and a section on “Safety and Precaution” that examines side effects, toxicity, and disease and drug interactions.
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The effect of feeding curcumin, capsaicin, ginger, mustard, black pepper and cumin on cholesterol and bile acid metabolism was studied in rats. The activity of hepatic cholesterol-7 alpha-hydroxylase, the rate-limiting enzyme of bile acid biosynthesis, was significantly elevated in curcumin (turmeric), capsaicin (red pepper), ginger and mustard treated animals. The enzyme activity was comparable to controls in black pepper and cumin fed rats. Serum and liver microsomal cholesterol contents were significantly higher in the curcumin and capsaicin treated animals. Thus, this study has suggested that the spices--turmeric, red pepper, ginger and mustard can stimulate the conversion of cholesterol to bile acids, an important pathway of elimination of cholesterol from the body. However, simultaneous stimulation of cholesterol synthesis by the spice principles--curcumin and capsaicin suggests that there may not be any significant contribution of stimulation of bile acid biosynthesis to the hypocholesterolemic action of these spices, and the latter action may solely be due to interference with exogenous cholesterol absorption.
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The efficacy of ginger for the prevention of postoperative nausea and vomiting was studied in a double-blind, randomized, controlled trial in 108 ASA 1 or 2 patients undergoing gynaecological laparoscopic surgery under general anaesthesia. Patients received oral placebo, ginger BP 0.5g or ginger BP 1.0g, all with oral diazepam premedication, one hour prior to surgery. Patients were assessed at three hours postoperatively. The incidence of nausea and vomiting increased slightly but nonsignificantly with increasing dose of ginger. The incidence of moderate or severe nausea was 22, 33 and 36%, while the incidence of vomiting was 17, 14 and 31% in groups receiving 0, 0.5 and 1.0g ginger, respectively (odds ratio per 0.5g ginger 1.39 for nausea and 1.55 for vomiting). These results were essentially unchanged when adjustment was made for concomitant risk factors. We conclude that ginger BP in doses of 0.5 or 1.0 gram is ineffective in reducing the incidence of postoperative nausea and vomiting.
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Antioxidant activities of the rhizomes of nine tropical gingers (Curcuma aeruginosa, Curcuma domestica, Curcuma heyneana, Curcuma mangga, Curcuma xanthorrhiza, Zingiber cassumunar, Phaeomeria speciosa, Alpinia galanga, and Amomum kepulaga) have been measured by thiocyanate and TBA methods in a water/alcohol system after extraction and fractionation with organic solvents. The quantity of three known curcuminoids, one of the potent antioxidant family of ginger species, in the extracts has been analyzed by HPLC. The antioxidant activity of the extracts of the gingers was greater than that estimated from the actual quantity of three known curcuminoids in the extracts.
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Polyunsaturated fatty acids (PUFA) are vulnerable to peroxidative attack. Protecting PUFA from peroxidation is essential to utilize their beneficial effects in health and in preventing disease. The antioxidants vitamin E, t-butylhydroxy toluene (BHT) and t-butylhydroxy anisole (BHA) inhibited ascorbate/Fe(2+)-induced lipid peroxidation in rat liver microsomes. In addition, a number of spice principles, for example, curcumin (5-50 microM) from turmeric, eugenol (25-150 microM) from cloves and capsaicin (25-150 microM) from red chillies inhibited lipid peroxidation in a dose-dependent manner. Zingerone from ginger inhibited lipid peroxidation at high concentrations (greater than 150 microM) whereas linalool (coriander), piperine (black pepper) and cuminaldehyde (cumin) had only marginal inhibitory effects even at high concentrations (600 microM). The inhibition of lipid peroxidation by curcumin and eugenol was reversed by adding high concentrations of Fe2+.
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The effect of powdered ginger root was compared with metoclopramide and placebo. In a prospective, randomised, double-blind trial the incidence of postoperative nausea and vomiting was measured in 120 women presenting for elective laparoscopic gynaecological surgery on a day stay basis. The incidence of nausea and vomiting was similar in patients given metoclopramide and ginger (27% and 21%) and less than in those who received placebo (41%). The requirement for postoperative antiemetics was lower in those patients receiving ginger. The requirements for postoperative analgesia, recovery time and time until discharge were the same in all groups. There was no difference in the incidence of possible side effects such as sedation, abnormal movement, itch and visual disturbance between the three groups. Zingiber officinale is an effective and promising prophylactic antiemetic, which may be especially useful for day case surgery.
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Effect of spice principles on scavenging of superoxide anion has been investigated. The superoxide anions, as measured by nitrobluetetrazolium (NBT) reduction in xanthine-xanthine oxidase system, were inhibited by superoxide dismutase, spice principles eugenol (cloves) and cuminaldehyde (cumin), antioxidants, butylated hydroxy toluene and butylated hydroxyanisole in a dose-dependent manner. The K(i) values for the inhibition of NBT reduction by eugenol and cuminaldehyde were 64 microM and 120 microM respectively. Zingerone (ginger) and linalool (coriander) inhibited NBT reduction to a maximum of 23 and 28% respectively. However, piperine (black pepper) and turmeric extracts (aqueous and acid) failed to scavenge superoxide anions.
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We previously reported on the isolation and identification of (E)-8 beta,17-epoxylabd-12-ene-15,16-dial (ZT) from ginger (rhizome of Zingiber officinale Roscoe, Zingiberaceae). In this paper, the pharmacological effects of ZT are reported. The experimental mouse hypercholesterolemia induced by Triton WR-1339 was treated after oral administration of ZT. In homogenated rat liver with ZT, cholesterol biosynthesis was decreased. In addition, the same activity was observed in the homogenated rat liver which was resected after the oral administration of ZT. According to the results of general pharmacological screening, no remarkable activity of ZT was observed except for an inhibitory effect on the cholesterol biosynthesis.
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Inhibitors of cholesterol biosynthesis are believed to lower serum cholesterol levels by enhancing the removal of serum low-density lipoprotein (LDL) by increasing hepatic LDL receptor function. Thus, the effects of several different inhibitors of cholesterol biosynthesis were examined for their effects on the expression of the hepatic LDL receptor in rats. We found that administration of inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase such as lovastatin, pravastatin, fluvastatin, and rivastatin resulted in increased hepatic LDL receptor mRNA levels. Surprisingly, these agents failed to increase levels of immunoreactive LDL receptor protein in rat liver even when the dose and length of treatment were increased. Treatment of rats with zaragozic acid A, an inhibitor of squalene synthase, caused even greater increases in hepatic LDL receptor mRNA levels, but did not increase levels of immunoreactive protein. Further investigation revealed that the rate of degradation of the hepatic LDL receptor was increased in rats given inhibitors of cholesterol biosynthesis. The greatest increase in the rate of degradation was seen in animals treated with zaragozic acid A which caused the largest increase in hepatic LDL receptor mRNA levels. In contrast, hepatic LDL receptor protein was stabilized in cholesterol-fed rats. It appears that increased potential for LDL receptor protein synthesis, reflected in increased mRNA levels, is offset by a corresponding increase in the rate of receptor protein degradation resulting in constant steady-state levels of hepatic LDL receptor protein. These findings are suggestive of increased cycling of the hepatic LDL receptor. This postulated mechanism can provide for enhanced hepatic uptake of lipoproteins without increasing steady-state levels of LDL receptor protein.