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Honey is the only insect-derived natural product with therapeutic, traditional, spiritual, nutritional, cosmetic, and industrial value. In addition to having excellent nutritional value, honey is a good source of physiologically active natural compounds, such as polyphenols. Unfortunately, there are very few current research projects investigating the nootropic and neuropharmacological effects of honey, and these are still in their early stages. Raw honey possesses nootropic effects, such as memory-enhancing effects, as well as neuropharmacological activities, such as anxiolytic, antinociceptive, anticonvulsant, and antidepressant activities. Research suggests that the polyphenol constituents of honey can quench biological reactive oxygen species and counter oxidative stress while restoring the cellular antioxidant defense system. Honey polyphenols are also directly involved in apoptotic activities while attenuating microglia-induced neuroinflammation. Honey polyphenols are useful in improving memory deficits and can act at the molecular level. Therefore, the ultimate biochemical impact of honey on specific neurodegenerative diseases, apoptosis, necrosis, neuroinflammation, synaptic plasticity, and behavior-modulating neural circuitry should be evaluated with appropriate mechanistic approaches using biochemical and molecular tools.
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Review Article
Neurological Effects of Honey: Current and Future Prospects
Mohammad Mijanur Rahman,1Siew Hua Gan,2and Md. Ibrahim Khalil1
1Department of Biochemistry and Molecular Biology, Jahangirnagar University, Savar, Dhaka 1342, Bangladesh
2Human Genome Centre, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia
Correspondence should be addressed to Md. Ibrahim Khalil;
Received  January ; Accepted  March ; Published  April 
Academic Editor: Pasupuleti Visweswara Rao
Copyright ©  Mohammad Mijanur Rahman et al. is is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
Honey is the only insect-derived natural product with therapeutic, traditional, spiritual, nutritional, cosmetic, and industrial value.
In addition to having excellent nutritional value, honey is a good source of physiologically active natural compounds, such as
polyphenols. Unfortunately, there are very few current research projects investigating the nootropic and neuropharmacological
eects of honey, and these are still in their early stages. Raw honey possesses nootropic eects, such as memory-enhancing eects, as
well as neuropharmacological activities, such as anxiolytic, antinociceptive, anticonvulsant, and antidepressant activities. Research
suggests that the polyphenol constituents of honey can quench biological reactive oxygen species and counter oxidative stress
while restoring the cellular antioxidant defense system. Honey polyphenols are also directly involved in apoptotic activities while
attenuating microglia-induced neuroinammation. Honey polyphenols are useful in improving memory decits and can act at the
molecular level. erefore, the ultimate biochemical impact of honey on specic neurodegenerative diseases, apoptosis, necrosis,
neuroinammation, synaptic plasticity,and behavior-modulating neural circuitry should be evaluated with appropriate mechanistic
approaches using biochemical and molecular tools.
1. Introduction
Honey, a natural food product, is a sweet, viscous substance
that is formed from the nectar of owers by honeybees
(Apis mellifera; Family: Apidae). e conversion of nectar
to honey is an impressively complex process. Nectar is rst
collected from owers and undergoes ripening by partial
enzymatic digestion in the honey stomach of the honeybee.
e ripened nectar is then matured by moisture evaporation
through fanning by the bees, which leaves a moisture content
of only approximately  to % in the honey []. Honey
civilization appeared approximately , years ago. Most
ancient civilizations, such as the Egyptians, Greeks, Chinese,
Mayans, Romans, and Babylonians, used honey both for
nutritional purposes and for its medicinal properties [].
Honey is the only insect-derived natural product, and it has
therapeutic, religious, nutritional, cosmetic, industrial, and
traditional value.
e global production of honey increased by %, from
,, to ,, tons, between  and  [].
In addition to the consumption of raw honey, the use of
honey in beverages is also increasing in popularity. Although
modern science has reported its medical benets, honey
has historically been utilized in various food products as a
sweetening agent and in medicine as a therapeutic agent for
woundhealingandforthetreatmentofcataracts[,]. Raw
honey has been used for centuries by traditional medical
practitioners worldwide in numerous medical treatments,
such as treatments for eye diseases in India, cough and sore
throat in Bangladesh, leg ulcers in Ghana, and measles in
Nigeria [].
e traditional knowledge of honey and modern sci-
ence are merged in “apitherapy,” which denotes the medical
use of honey and bee products. Apitherapy has become
a major focus of research involving alternative medicine
because a wide variety of well-known preventive or curative
methods from folk medicine use honey to treat dierent
ailments, and the therapeutic properties of honey have been
increasingly documented in the modern scientic literature
[]. Recently, the oral ingestion of raw honey has been
indicated for insomnia, anorexia, stomach and intestinal
Hindawi Publishing Corporation
Evidence-Based Complementary and Alternative Medicine
Volume 2014, Article ID 958721, 13 pages
Evidence-Based Complementary and Alternative Medicine
T : An overview of composition of raw honey [].
Nutrient Value in  g
Moisture . g
Carbohydrate . g
Glucose . g
Fructose . g
Sucrose . g
Maltose . g
Galactose . g
Total dietary ber . g
Protein . g
Total lipid (fat) . g
Ash . g
Energy  kcal
ulcers, constipation, osteoporosis, and laryngitis. Externally
applied honey is used to treat athlete’s foot, eczema, lip sores,
and both sterile and infected wounds caused by accidents,
surgery, bedsores, or burns. In many countries, including
France and Germany, physicians recommend using honey as
a rst-line treatment for burns, supercial wounds, and in
some cases, even deep lesions such as abscesses [].
2. Nutritional Facts about Honey
To date, approximately  varieties of honey have been
identied []. ese varieties exist due to the variable types
of nectar that are collected by the honeybees. Although there
have been many nutritional studies of honey, only a few are
representative. Carbohydrates are the main constituents of
honey and contribute  to % of its dry weight. In addition
to carbohydrates, honey contains numerous compounds,
such as organic acids, proteins, amino acids, minerals, and
vitamins [,](Table). Pure honeys were also reported
to contain polyphenols, alkaloids, anthraquinone glycosides,
cardiac glycosides, avonoids, reducing compounds, and
volatile compounds [].
Monosaccharides, such as fructose and glucose, are the
predominant sugars present in honey, and they are said
to be responsible for most of the physical and nutritional
characteristics of honey [].Smallerquantitiesofother
types of sugars, such as disaccharides, trisaccharides, and
oligosaccharides, are also present in honey. e disaccharides
primarily include sucrose, galactose, alpha,beta-trehalose,
gentiobiose, and laminaribiose, whereas the trisaccharides
primarily include melezitose, maltotriose, -ketose, panose,
isomaltose glucose, erlose, isomaltotriose, theanderose, cen-
tose, isopanose, and maltopentaose []. Approximately
 to % of total carbohydrates are oligosaccharides, and
approximately  dierent oligosaccharides have been identi-
ed [,]. Many of these sugars are not found in the nectar
but are formed during the honey ripening and maturation
Gluconic acid, which is a product of glucose oxidation by
glucose oxidase, is the major organic acid that is found in
honey; in addition, minor amounts of formic, acetic, citric,
lactic, maleic, malic, oxalic, pyroglutamic, and succinic acids
have also been detected []. ese organic acids contribute
to the acidic (pH between . and .) characteristic of honey
[]. However, honey can also behave as a buer.
Honey also contains several physiologically important
amino acids, including all nine essential amino acids and
all nonessential amino acids except for glutamine and
asparagine. Among the amino acids present, proline is
predominant, followed by aspartate, glutamate, and some
other types of amino acids []. However, in another study,
proline was reported as the primary amino acid in honey,
followed by lysine []. Enzymes that are either secreted from
botanical nectars constitute the main protein component of
honey. ese enzymes include the bee hypopharyngeal gland-
derived diastase (an amylase that digests starch to maltose),
invertases (e.g., saccharase and 𝛼-glucosidase that catalyzes
the conversion of sucrose to glucose and fructose), glucose
oxidase (which produces hydrogen peroxide and gluconic
acid from glucose), and plant-derived catalase (which regu-
lates the production of hydrogen peroxide), along with acid
phosphatase [].
e vitamin content in honey is generally low and does
not meet the recommended daily intake (RDI). Usually, all of
the water-soluble vitamins are present in honey, with vitamin
C being the most abundant. Approximately  dierent
minerals have been detected in honey, including all of the
major minerals, such as calcium, phosphorus, potassium,
sulfur, sodium, chlorine, and magnesium (Table ). Some
honey, such as rubidium (RB), silicon (Si), zirconium (Zr),
vanadium (V), lithium (Li), and strontium (Sr), as well as
some trace elements, such as lead (Pb), cadmium (Cd),
and arsenic (As), which could be present due to contami-
nants from surrounding environments []. Interestingly, the
amounts of these minerals follow a geographical variation;
the mineral compositions of honeys that are collected from
similar regions are similar. However, several previous reports
whereas several other recent reports suggest that honey is rich
in minerals [,]. Essential trace elements are important,
particularly among growing children because of their rapid
the RDI clearly indicates that honey contains a substantial
amount of several essential trace elements that would par-
tially meet the RDI for children (Table ). For adults, honey
is a good source of potassium.
3. Other Nonnutritional
Components of Honey
Previous studies have reported the presence of approximately
 dierent volatile compounds in honey, and these com-
pounds can be used to characterize its botanical source
[]. In addition, volatile compounds can also impart aro-
matic characteristics to honey and contribute to its potential
biomedical activity []. e volatile composition of honey is
generally low but includes hydrocarbons, aldehydes, alcohols,
Evidence-Based Complementary and Alternative Medicine
T : A comparison of the minerals found in honey (major and essential trace minerals) with RDI as reported from several studies [].
Major minerals RDI One tablespoon ( g) Essential trace minerals RDI One tablespoon ( g)
Calcium  mg . mg [] Copper  mg . mg []
Chloride  mg . mg [] Fluoride  𝜇g . 𝜇g[]
Magnesium – mg . mg [] Iron – mg . mg []
Phosphorus  mg . mg [] Molyb denum  𝜇g . 𝜇g[]
Potassium  mg . mg []Selenium𝜇g . 𝜇g[]
Sodium  mg . mg [] Zinc  mg . mg []
e values are daily reference values (DRVs) of RDI. e DRVs for major minerals are based on a caloric intake of , calories for adults and children (of
four or more years of age). For trace elements, the RDIs that are given are the maximums for all sex and age groups [,].
ketones, acid esters, benzene and its derivatives, furan and
pyran, norisoprenoids, terpene and its derivatives, and sulfur,
as well as cyclic compounds [,].
Polyphenols and avonoids, which act as antioxidants,
are two important bioactive molecules that are present in
honey. Emerging evidence from recent studies has conrmed
the presence of approximately  dierent polyphenols in
honey [,]. e total polyphenol content of honey varies
from  to  mg/kg, whereas the avonoid content varies
from  mg/kg to  mg/kg [,,]. e presence and
concentrations of these polyphenols in honeys can vary
depending upon the oral source and the geographical and
climatic conditions. Some bioactive compounds, such as
Galangin, kaempferol, quercetin, isorhamnetin, and luteolin,
are present in all types of honey, whereas others, such as
hesperetin and naringenin, are reported only in specic
varieties []. Overall, the most commonly reported phenolic
and avonoid compounds in honey include ellagic acid,
gallic acid, syringic acid, benzoic acid, cinnamic acid, ferulic
acids, chlorogenic acid, caeic acid, coumaric acid, myricetin,
chrysin, hesperetin, isorhamnetin, quercetin, galangin, api-
genin, catechin, kaempferol, naringenin, and luteolin [,,
4. Effects of Honey on Brain
Structures and Functions
4.1. Current Experimental Evidence of the Nootropic and
Neuropharmacological Eects of Honey. Research from the
past two decades has explored honey as an enigmatic gel
that has gastroprotective, hepatoprotective, reproductive,
hypoglycemic, antioxidant, antihypertensive, antibacterial,
antifungal, anti-inammatory, immunomodulatory, wound
healing, cardio-protective and antitumor eects [,,,
]. Unfortunately, research on the nootropic and neurophar-
macological eects of honey is scarce. Nevertheless, the
belief that honey is a memory-boosting food supplement is
actually ethnotraditional as well as ancient in nature. For
instance, honey is reported to be an important component of
Brahma rasayan, an Ayurvedic formulation that is prescribed
to extend the lifespan and improve memory, intellect, con-
centration, and physical strength [].
One established nootropic property about honey is that
it assists the building and development of the entire central
nervous system, particularly among newborn babies and
preschool age children, which leads to the improvement
of memory and growth, a reduction of anxiety, and the
enhancement of intellectual performance later in life [].
Additionally, the human brain is known to undergo postnatal
development with the obvious maturation and reorganization
cortex. It has been reported that this postnatal development
occurs through neurogenesis, which occurs predominantly
during childhood, and this development can also extend into
adolescence and even through adulthood []. Empirical,
but striking, evidence supporting this concept was provided
by an experiment that was conducted on postmenopausal
women; those who received honey showed improvements in
their immediate memory but not in immediate memory aer
interference or in delayed recall []. In another study, the
normal diet of two-month-old rats was supplemented with
honey, and their brain function was assessed over a one-
year period. Honey-fed rats showed signicantly less anxiety
and better spatial memory throughout all stages compared
with the control group of rats. More importantly, the spatial
memory of honey-fed rats, as assessed by object recognition
tasks, was signicantly greater during later months (i.e.,  and
) [].
In agreement with the previous study, both short-
and long-term supplementations with honey at a dose of
 mg/kg body weight signicantly decreased the lipid per-
oxidation in brain tissue with a concomitant augmentation
of superoxide dismutase (SOD) and glutathione reductase
activity. us, honey consumption ameliorates the defense
mechanism against oxidative stress and attenuated free
radical-mediated molecular destruction []. Furthermore,
honey decreased the number of degenerated neuronal cells
in the hippocampal CA region, a region that is known to
behighlysusceptibletooxidativeinsult[]. eoretically,
the cumulative macromolecular destruction by free radicals
due to an imbalance between the prooxidant and antioxidant
defense systems is implicated in aging []. Many studies
have focused on the evidence of oxidative stress in neurode-
generative diseases, such as Alzheimer’s disease (AD), mild
cognitive impairment, Parkinsons disease (PD), amyotrophic
lateral sclerosis (ALS), and Huntingtons disease (HD) [].
Emerging research has documented the neuropharma-
al. [] conducted the rst such study, in which rats were
fed with dierent concentrations of honey (,  and
%) at a dose of . mL/ g. Signicant dose-dependent
Evidence-Based Complementary and Alternative Medicine
increases in exploratory activities in a hole board test and in
locomotor, rearing and grooming activities in an open-eld
test were found in the honey-fed test groups rats compared
with the control group rats. ese ndings indicate that
the consumption of honey mitigates anxiety and exerts an
excitatory eect on the central nervous system, especially
at the highest nonsedative dose []. In another study, the
neurological eects of honey were investigated by assessing
spatial working memory in mice using () the Y-maze test
and () pentobarbital-induced hypnosis and assessing, ()
its anxiolytic activities using hole-board and elevated plus-
maze tests, () its anticonvulsant activity in an picrotoxin
seizure model, () its antinociceptive activity in hot-plate and
tail-ick tests, and () its antidepressant eects using the
forced swimming test. e authors of that study concluded
that honey is a functional food that possesses anxiolytic,
antinociceptive, anticonvulsant, and antidepressant eects
Indeed, the neuropharmacological impact of honey
reects the preliminary modulatory ability of the neural
circuit and associated neurochemical systems that underlie
the behavioral and molecular changes associated with the
experimental paradigm. ese insights into the neurophar-
macological eects of honey highlight the neurological fac-
tors that are inuenced by treatment with honey. Exploratory
behaviors oen involve the excitatory neural systems, such
as the cholinergic and dopaminergic systems, whereas anx-
ious behavior oen involves the inhibitory neural system,
specically 𝛾-aminobutyric acid (GABA) []. Several
lines of experimental evidence support the hypothesis that
the neuropharmacological eects of honey are mediated via
dopaminergic and nonopioid central mechanisms, such as
the voltage-gated sodium channel blocking hypothesis, the
activation of the noradrenergic inhibitory system and/or
serotonergic systems, and the GABAergic system [,].
In addition to neural eects, glial cells may also respond
to honey therapy because honey shows a neuroprotective
eect in the cerebral focal-induced ischemia model in rats
[]. Moreover, honey attenuated ischemia-induced neuroin-
ammation by activating microglia, and neuroinammatory
processes in the brain are believed to play a crucial role in
the development of neurodegenerative diseases as well as in
neuronal injury associated with stroke [,]. Interestingly,
ischemia-induced cognitive impairments that result from
microglia- and/or astrocyte-mediated neuroinammation
were also signicantly attenuated by honey therapy [,].
5. The Effects of Physiologically Active
Moieties in Honey on Brain Function
Oxidative stress is a common manifestation of all types of
biochemical insults to the structural and functional integrity
of neural cells, such as aging, neuroinammation, and neu-
rotoxins. e brain is highly susceptible to oxidative damage
due to its high oxygen demand as well as to the high amount
of polyunsaturated fatty acids (PUFAs) in the neuronal
membranes []. Dierent phytochemical compounds have
been shown to have scavenging activities and can activate
key antioxidant enzymes in the brain, thus breaking the
vicious cycle of oxidative stress and tissue damage [,].
Several supplementary research reports have suggested that
the neuroprotective eect of the polyphenols present in
honey involves several important activities within the brain.
ese eects include protection against oxidative challenge;
the attenuation of neuroinammation; the promotion of
memory, learning, and cognitive function; and protection
against neurotoxin-induced neuronal injury. We describe
several important constituents in honey that may play this
protective role.
Apigenin is a common avonoid that is frequently identi-
ed in honey. In addition to its radical scavenging activity,
apigenin protects neurons against oxygen-glucose depriva-
tion/reperfusion-induced injury in cultured primary hip-
pocampal neurons by improving sodium/potassium-ATPase
(Na+/K+-ATPase) activities []. Apigenin also inhibits the
kainic acid-induced excitotoxicity of hippocampal cells in
a dose-dependent manner by quenching reactive oxygen
species and by inhibiting the depletion of reduced glutathione
(GSH) levels []. Apigenin suppresses the interferon gamma
(IFN-𝛾)-induced expression of CD, whereas the signaling
of CD is critically involved in microglia-related immune
responses in the brain. Rezai-Zadeh et al. suggested that
apigenin may have neuroprotective and disease-modifying
properties in several types of neurodegenerative disorders
[]. Moreover, apigenin stimulates the adult neurogenesis
that underlies learning and memory [].
Caeic acid, another important antioxidant, is a type of
phenolic acid that is present in honey, as well as in coee,
fruits and vegetables. An in vitro study has demonstrated
the neuroprotective eects of caeic acid on neuronal cells
[]. e neuroinammatory suppression activity of caf-
feic acid can be inferred from the observation that caeic
acid reverses the aluminum-induced overexpression of -
lipoxygenase (-LOX) in brain tissues []. Caeic acid also
is associated with neuronal death in the hippocampus and
with learning and memory decits []. In vitro treatment
with caeic acid at several dierent concentrations has been
reported to increase the acetylcholinesterase activity in the
cerebral cortex, cerebellum, and hypothalamus. A similar
scenario is also observed in the cerebellum, hippocampus,
hypothalamus, and pons when caeic acid is administered in
vivo. All of these ndings strongly support the proposition
that caeic acid improves memory by interfering with cholin-
ergic signaling, in addition to its neuroprotective eects [].
Catechin is a avonoid that contributes to the antioxidant
activities of honey. Several studies have repeatedly demon-
strated the neuroprotective eects of catechin on neuronal
death in a wide array of cellular and animal models of neuro-
logical diseases [,]. Although catechin possesses potent
iron-chelating, radical-scavenging, and anti-inammatory
activities, current studies have indicated that the modulation
of signal transduction pathways, cell survival, or death genes
and mitochondrial function signicantly contribute to the
induction of cell viability []. For instance, according to
Unno et al., the daily consumption of green tea, which con-
tains high levels of catechin, can delay the memory regression
Evidence-Based Complementary and Alternative Medicine
that is associated with age-related brain atrophy and cognitive
dysfunction []. Animal studies have indicated that the
long-term administration of green tea may prevent age-
related learning and memory decline by modulating the
transcription factor cAMP-response element binding pro-
tein (CREB) and by upregulating synaptic plasticity-related
proteins in the hippocampus [,]. Similar memory-
ameliorating eects were also shown in the context of
neurodegenerative diseases, such as PD, AD, and multiple
sclerosis [].
Chlorogenic acid is a derivative of caeic acid and is
another common phenolic acid that is found in honey. A
dose-dependent protective eect of chlorogenic acid against
apoptosis was observed in pheochromocytoma- (PC)
cell lines that were exposed to methyl mercury-induced
apoptotic damage. e protective activity of chlorogenic acid
was associated with a reduction in the generation of reactive
oxygen species (ROS) and the attenuation of apoptosis by the
activation of caspase- []. In a study by Kwon et al. [], the
neuroprotective eects of chlorogenic acid on scopolamine-
induced learning and memory impairment were investigated
using several behavioral tests, such as the Y-maze, passive
avoidance, and Morris water maze tests. Chlorogenic acid was
found to signicantly improve memory-related performance
in all of the tests. It was concluded that chlorogenic acid
may exert antiamnesic activity via the inhibition of acetyl-
cholinesterase and malondialdehyde in the hippocampus
and frontal cortex because chlorogenic acid inhibited the
acetylcholinesterase activity of the hippocampus and frontal
cortex in both ex vivo and in vitro model systems []. Chloro-
genic acid inhibits the synthesis and release of inammatory
mediators, such as tumor necrosis alpha and nitric oxide
(NO), thus contributing to anti-inammatory and analgesic
activities against carrageenan-induced inammation [].
erefore, the chlorogenic acid in honey might have the
capacity to attenuate neuroinammation.
Chrysin (,-dihydroxyavone) is another important
avonoid antioxidant that is present in honey. A behavioral
experimental model revealed that chrysin is an anxiolytic
that acts as a central receptor for benzodiazepine in instances
where anxiety was reported to hamper cognitive function
and learning capacity []. A study conducted by He et
al. [] showed that the therapeutic potential of chrysin
in neurodegeneration-associated dementia resulted from
cerebral hypoperfusion. e eects of chrysin were further
investigated in a rat model of cognitive decits and brain
damage generated by the permanent occlusion of the bilat-
eral common carotid arteries []. Such surgically induced
hypoperfusion leads to a signicant increase in the escape
latency in the Morris water maze, with biochemical features
of neural damage, such as increases in glial brillary acidic
protein expression and apoptosis. Interestingly, chronic treat-
ment with chrysin signicantly alleviated neuronal damage
and spatial memory decits, with a reduction in lipid per-
oxidation and glutathione peroxidase activity but a decrease
in SOD activity [], indicating the neuroprotective role of
p-Coumaric acid is the most abundant of the three
hydroxy derivatives of cinnamic acid. A previous study
demonstrated the oxidative stress reduction capacity
and antigenotoxic capacity of p-coumaric acid []. In
doxorubicin-induced cardiotoxicity, p-coumaric acid was
able to increase the levels of GSH, SOD, and catalase activities
with a concomitant reduction of lipid peroxidation [].
p-Coumaric acid exhibited neuroprotective eects against
-S-cysteinyl-dopamine-induced neurotoxicity. e extent
to which p-coumaric acid confers neuroprotection was
reported to be equal to or greater than that observed for the
avonoids (+)-catechin, ()-epicatechin, and quercetin [].
Ellagic acid is a phenolic acid that is found not only
in fruits and vegetables but also in honey. In addition to
its antioxidant activity, ellagic acid exerts chemopreventive
eects, as indicated by its antiproliferative activity [].
Interestingly, the chemopreventive eects of ellagic acid are
executed through the reduction of oxidative stress at the
cellular level []; moreover, oxidative stress is involved in
neurodegeneration and age-related memory decits. Hence,
ing. Treatment with ellagic acid also restores the levels of
lipid peroxides and NO (nitric oxide), the activities of catalase
and paraoxonase, and the total antioxidant status of the
brain to normal levels []. Other experiments also support
the hypothesis that ellagic acid reduces oxidative stress in
the brain, which is reected by improvements in cognitive
function. Ferulic acid, another polyphenol that is found in
honey, is a phenolic acid. Ferulic acid can provide neu-
roprotection against cerebral ischemia/reperfusion injury-
associated apoptosis in rats. Ferulic acid treatment resulted
in a decrease of the extent of apoptosis, with decreased
levels of ICAM- mRNA and reduced numbers of microglia
and macrophages. is phenomenon ultimately results in
the downregulation of inammation-induced oxidative stress
and oxidative stress-related apoptosis []. In another study
[], the ameliorating eects of ferulic acid on apoptosis
caused by cerebral ischemia or reperfusion were investigated.
p mitogen-activated protein (MAP) kinase-mediated NO-
induced apoptosis. It was also reported that ferulic acid
inhibits Bax translocation, the release of cytochrome c,
and p MAP kinase phosphorylation and enhances the
expression of the GABAB receptor []. Ferulic acid could
also alleviate learning and memory decits through the
concomitant inhibition of acetylcholinesterase activity and
the augmentation of SOD activity while lowering the con-
centration of glutamic acid and malondialdehyde in the hip-
pocampus of rats. ese results suggested that the antioxidant
activities of the honey may contribute to the improvement
of the cholinergic system in the brain or to the inhibition
of nerve injury by excitatory amino acids []. Ferulic acid
may be useful for preventing trimethyltin-induced cognitive
dysfunction as well as for boosting the activation of choline
acetyltransferase (ChAT) in dementia [].
Gallic Acid. Gallic acid prevents the apoptotic death
of cortical neurons in vitro by inhibiting amyloid beta
(–)-induced glutamate release and the generation of
ROS []. Gallic acid possesses an antianxiolytic activity,
which provided the primary evidence in support of
Evidence-Based Complementary and Alternative Medicine
the memory-ameliorating eect of gallic acid because
anxiety is associated with memory disturbance []. e
memory-ameliorating eects of gallic acid were further
conrmed by Al Mansouri et al. [], who revealed its
neuroprotective eect on -hydroxydopamine-induced and
cerebral oxidative stress-induced memory decits. Gallic acid
improved memory concomitant with increases in the total
thiol pool and glutathione peroxide activity and decreased
lipid peroxidation in the hippocampus and striatum [].
However, we cannot claim that these biochemical ndings
are entirely responsible for the improvements in memory.
Kaempferol is a plant avonoid that is also frequently
found in honey. e toxicity of -methyl--phenyl-,,,-
tetrahydropyridine (MPTP), which is a neurotoxin, leads
to behavioral decits, a depletion of dopamine, reductions
in SOD and glutathione peroxidase activities, and an ele-
vation of lipid peroxidation in the substantia nigra. e
administration of kaempferol has been reported to reverse
all of these behavioral and biochemical alterations and to
prevent the loss of TH-positive neurons that is induced by
MPTP (-methyl--phenyl-,,,-tetrahydropyridine) [].
In another study, kaempferol demonstrated the ability to
protect primary neurons from rotenone-induced apoptotic
challenge. Specically, kaempferol-ameliorated antioxidant
defenses and antiapoptotic eects involve the enhancement
of mitochondrial turnover, which is mediated by autophagy
[]. Furthermore, kaempferol may be an optimal treatment
for improving cognitive function due to its positive eects on
depression, mood, and cognitive functions [].
Luteolin is a avonoid from the avone class that has
been reported to be found in honey. As is the case for most
avonoids, luteolin has antioxidant, anti-inammatory, and
antitumor properties []. Luteolin also has neuroprotec-
tive eects against microglia-induced neuronal cell death.
e consumption of luteolin has been found to improve
the spatial working memory of aged rats by mitigating
microglia-associated inammation in the hippocampus [].
e impairment of learning acquisition induced by cholin-
ergic neurotoxins and muscarinic and nicotinic receptor
antagonists were reported to be attenuated by luteolin. is
phenomenon, however, was not observed for dopaminergic
neurotoxin- and serotonergic neurotoxin-induced memory
impairments, thus conrming the involvement of the central
cholinergic system in the memory-restoring function of
luteolin [].
Interestingly, Tsai et al. showed that the augmenting
eect of luteolin on Mn-SOD and (Cu/Zn)-SOD activity as
well as on the GSH levels in the cortex and hippocampus
was associated with the amelioration of amyloid beta (–
)-induced oxidative stress and cognitive decits [].
Luteolin is believed to enhance basal synaptic transmission
and facilitate the induction of long-term potentiation (LTP)
by high-frequency stimulation in the dental gyrus of the
hippocampus. At the molecular level, the LTP inductive eect
of luteolin involves the activation of cAMP response element-
binding protein (CREB) [].
Myricetin is another well-known avonoid that has
also been reported to be found in honey. Yasuo et al.
() demonstrated that myricetin can reduce the calcium-
induced increase in oxidative metabolism in rat brain neu-
rons when administered at a concentration of  nM or
greater []. In the case of the retinoid-induced apoptosis
of human neuroblastoma cells, myricetin induced neuropro-
tection through a protective eect against retinoid-induced
oxidative stress. e neuroprotective eect of myricetin was
reported to be associated with a reduction in lipid per-
oxidation, retinoid-induced hydrogen peroxide generation,
and superoxide radical generation (O2−), as well as an
elevation of the glutathione redox status []. In another
study, myricetin was also reported to signicantly prevent
D-galactose-induced cognitive impairment. e results of
this study also indicated that cognitive impairment was
most likely mediated by the extracellular signal-regulated
kinase- (ERK-) cyclic AMP response element binding
protein (CREB) signaling pathway in the hippocampus
Naringenin can confer a neuroprotective eect against
quinolinic acid-induced excitotoxicity mediated by elevated
intracellular calcium levels, NO-mediated oxidative stress,
and, consequently, cell death []. Amyloid beta-protein-
induced free radical-mediated neurotoxicity is also attenu-
ated by naringenin []. Interestingly, free radical-mediated
loid beta- and quinolinic acid-induced neurotoxicity, and it
has repeatedly been implicated in neurodegeneration and
cognitive decits. In a rat model, the administration of
naringenin reversed the learning, memory, and cognitive
impairments caused by the intracerebroventricular admin-
istration of streptozotocin []. Treatment with naringenin
also increases the pool of GSH and the activities of glu-
tathione peroxidase, glutathione reductase, glutathione-S-
transferase, SOD, and choline acetyltransferase in the hip-
pocampus in a rat model of Alzheimer’s disease- (AD-)
type neurodegeneration with cognitive impairment (AD-
TNDCI), with a concomitant decrease in the loss of ChAT-
positive neurons and impairments in spatial learning and
memory [].
Quercetin is another avonoid with antioxidant activ-
ity that is commonly found in honey. An in vitro study
demonstrates that quercetin can inhibit oxidative insults as
well as oxidative stress-dependent and independent apop-
tosis in a neural cell model [,]. Quercetin improves
memory and hippocampal synaptic plasticity in models of
memory impairment that is caused by chronic lead exposure
[]. Quercetin also exhibited neuroprotective eects against
colchicine-induced cognitive impairments []. Another
neuroprotective role conrmed for quercetin is the allevi-
ation of neuroinammation. According to Sharma et al.,
quercetin modulates an interleukin- beta-mediated inam-
matory response in human astrocytes []. Quercetin also
decreases the extent of ischemic injury in a lesion-repeated
cerebral ischemic rat model and restores spatial memory
through the suppression of hippocampal neuronal death [,
on the peripheral nervous system and the central nervous
system (CNS). In another study, quercetin promoted the
Evidence-Based Complementary and Alternative Medicine
functional recovery of the spinal cord following acute injury
6. Honey as a Neuroprotective Nutraceutical
Generally, neurodamaging insults are categorized as either
endogenous or exogenous in nature. Because the neurons
of the mature nervous system are postmitotic, they cannot
be easily replaced by cell renewal; therefore, neuronal cell
death is the most widely studied neuronal pathologies.
Neurodegeneration describes the progressive loss of neural
structure and function that culminates in neuronal cell death.
Acute neurodegeneration is usually caused by a specic or
traumatic event, such as cardiac arrest, trauma, or sub-
arachnoid hemorrhage, whereas chronic neurodegeneration
occurs within the context of a chronic disease state with
a multifactorial origin, such as AD, PD, HD, or amyloid
lateral sclerosis []. e biochemical events underlying
neurodegeneration include oxidative stress, mitochondrial
dysfunction, excitotoxicity, neuroinammation, misfolded
protein aggregation, and a loss of functionality []. e
ultimate fate of such a neurodamaging insult is neuronal
cell death through apoptosis, necrosis, or autophagy [].
erefore, oxidative stress, mitochondrial dysfunction, and
inammation are prime candidates for neuroprotection [].
Much research over the last few decades has established
nutraceuticals as neuroprotective agents. In addition to the
acute modulation of the antioxidant defense system, several
nutraceuticals can also modulate gene expression to confer
long-term protection [,]. Phytochemicals can also
modify cellular behaviors by inuencing receptor function
as well as by modulating intracellular events, such as cell-
signaling cascades [,]. Honey and its constituents can
ameliorate oxidative stress and oxidative stress-related eects.
e neuroprotective eects of honey are exerted at dierent
stages of neurodegeneration and play prominent roles in early
events (Figure ).
7. Honey as a Nootropic Nutraceutical
Learning and memory are the most exclusive and basic func-
tions of the brain. Synaptic plasticity is thought to be crucial
for information processing in the brain and underlies the
processes of learning and memory []. Synaptic plasticity
describes the capacity of neurons to change their eciency in
neuronal transmission in response to environmental stimuli
and plays an essential role in memory formation. Long-term
synaptic plasticity, or long-term potentiation (LTP), is the
molecular analog of long-term memory and is the cellular
model that underlies the processes of learning and memory
[,]. e induction, expression, and maintenance of LTP
involve a series of biochemical events []. LTP is induced by
the inux of calcium into postsynaptic neurons through a set
of receptors and/or channels and is usually followed by the
amplication of calcium levels due to the release of calcium
from the Ca2+/InsP3-sensitive intracellular store [,].
e expression of LTP involves the activation of
several calcium-sensitive enzymes, which include
calcium/calmodulin-regulated protein kinases (CaMKII
and CaMKIV), the cAMP-dependent protein kinase A
(PKA), protein kinase C (PKC), and MAPK/ERKs [,].
Signaling events downstream and enzyme activation
ultimately cause the initial expression and maintenance of
LTP. However, the long-term expression and maintenance
of LTP requires ecient gene expression. PKA may induce
changes in the expression of genes via the phosphorylation
of the transcription factor CREB. Phosphorylated CREB
activates the transcription of genes with an upstream cAMP
response element (CRE) []. e activation of CREB via
MAPK/ERKs is thought to be connected to PKA and PKC
signaling. Furthermore, CaMKII and CaMKIV may play
a role in the maintenance of LTP through its eects on
CREB phosphorylation []. Ultimately, CREB mediates
the transcription and expression of at least two sets of genes,
which include genes that regulate the transcription of other
genes, such as c-fos,c-jun,zif268,andEgr-3,andeector
genes, such as Arc,Narp,Homer,Cox-2,andRheb,that
directly act on cells to evoke dierent eects, including
plastic changes [].
Current research has claried only a portion of the
involvement of honey polyphenols in memory-related signal-
ing pathways. However, the overall body of knowledge clearly
suggests the neuroprotective roles of honey and several
supplementary experimental studies support its memory-
improving eects. Overall, honey or its bioactive constituents
memory-improving eects (Figure ).
8. Concluding Remarks and Future Prospects
e brain is the supervisory organ with critical functions,
such as body homeostasis maintenance, learning, and mem-
ory. Any neurodamaging insult leads to either the death or
the functional aberration of neural cells, which results in
neurodegeneration and the loss of motor function and the
executive functions of the brain, such as memory. ere is
strong scientic support for the development of nutraceutical
agents as novel neuroprotective therapies, and honey is
one such promising nutraceutical antioxidant. However, past
research paradigms did not evaluate the neuropharmacolog-
ical and nootropic eects of honey using appropriately in-
depth mechanistic approaches concerning biochemical and
molecular interventions.
Honey has an appreciable nutritional value. Raw honey
possesses anxiolytic, antinociceptive, anticonvulsant, and
antidepressant eects and improves the oxidative status of
the brain. Several honey supplementation studies suggest
that honey polyphenols have neuroprotective and nootropic
eects. Polyphenol constituents of honey quench biolog-
ical reactive oxygen species that cause neurotoxicity and
aging as well as the pathological deposition of misfolded
proteins, such as amyloid beta. Polyphenol constituents
of honey counter oxidative stress by excitotoxins, such
as kainic acid and quinolinic acid, and neurotoxins, such
as -S-cysteinyl-dopamine and -methyl--phenyl-,,,-
tetrahydropyridine. Honey polyphenols also counter direct
Evidence-Based Complementary and Alternative Medicine
injury Tra u ma
Oxidative stress
Neuronal cell death
Activation of Microglia
and/or Astrocyte
H & HP
Aberration of antioxidant
defense system
Improvement of
antioxidant defense
Executioner Caspase
Initiator Caspase
Activ ation
environmental toxins)
Executioner caspase
Initiator Caspase
Activation of microglia
and/or astrocyte
Executioner Caspase
Cellular and nuclear
Cell swelling and
Initiator caspase
H/HP ?
Neurotoxic inammatory
F : e putative neuroprotective mechanism of honey and its polyphenols. e generation of reactive oxygen species (ROS) and/or
reactive nitrogen species (RNS) increases irrespective of neurodamaging insults that lead to oxidative stress. e dysfunction of the
antioxidant defense system synergistically causes reactive species accumulation, leading to oxidative stress. e ultimate outcome of such
oxidative stress is neuronal cell death through an inammatory, apoptotic, or necrotic response [,,]. Honey (H) and its
polyphenol constituents (HP) can counter oxidative stress by limiting the generation of reactive species as well as by strengthening the
cellular antioxidant defense system. Honey and several honey polyphenols (apigenin, ferulic acid, and catechin) prevent neuronal cell death
by attenuating neuroinammation and apoptosis. However, the neuroinammatory responses overlap with apoptosis, and the role of honey
in necrotic cell death remains unclear. X = stop or prevent and + = improve or intensify.
apoptotic challenges by amyloid beta, methyl mercury-
induced, and retinoid. Raw honey and honey polyphenol
attenuate the microglia-induced neuroinammation that is
induced by ischemia-reperfusion injury or immunogenic
neurotoxins. Most importantly, honey polyphenols counter
neuroinammation in the hippocampus, a brain structure
that is involved in spatial memory. Honey polyphenols also
counter memory decits and induce memory formation at
the molecular level. Several studies suggest that the mod-
ulation of specic neural circuitry underlies the memory-
ameliorating and neuropharmacological eects of honey
Our information demands the evaluation of the benets
of raw honey and its individual constituents in specic
neurodegenerative diseases, such as AD, PD, and HD. e
ultimate biochemical impact of honey on mitochondrial
dysfunction, apoptosis, necrosis, excitotoxicity, and neuroin-
ammation should also be explored. Furthermore, explo-
ration of the actual cell signaling cascades that are asso-
ciated with synaptic plasticity may provide more specic
therapeutic interventions using honey. e eect of honey
on synaptic plasticity under normal and disease conditions
should also be determined. e neural circuits and receptors
Evidence-Based Complementary and Alternative Medicine
Calcium inux
Synaptic plasticity-related proteins
Neural cell
CRE Down stream genes
F : Putative nootropic mechanisms of honey and its polyphenols. Calcium inux via the N-methyl-D-aspartate receptor (NMDAR)
occurs during the initial phase of NMDAR-dependent LTP. e inductive phase follows CREB phosphorylation through MAPK/ERKs
signaling, which ultimately leads to the transcriptional regulation of synaptic plasticity-related proteins. Metabotropic receptors include
ligand-gated ion channels that promote calcium inux (AMPA receptor) and enzyme-coupled receptors (such as cholinergic, glutamate, and
dopamine receptors) that can trigger a second messenger (cAMP/cGMP) to activate downstream eector enzymes. e eector enzymes
nally modulate the activation of CREB []. Honey polyphenols (HP: luteolin, myricetin, catechin) modulate synaptic plasticity
through the activation of CREB by MAPK/ERKs and/or PKA-involved cellular signaling.
honey, such as anxiolytic, antinociceptive, anticonvulsant,
and antidepressant activities, should be examined in further
Conflict of Interests
e authors declare that there is no conict of interests
regarding the publication of this paper.
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... Dans les miels, l'acide organique le plus représenté est l'acide gluconique (dont la teneur est 50 fois plus élevée que celle des autres acides). Produit lors de l'oxydation du glucose par l'action de la glucose oxydase, il est en équilibre avec le delta-gluconolactone. (Mijanur Rahman et al., 2014;White et al., 1962). Cet équilibre entre les acides organiques et les lactones correspondantes (considérées alors comme des « réservoirs d'acides ») confère au miel la capacité de retrouver son acidité originelle après une neutralisation (White, 1957;White et al., 1962 ;Bogdanov, 2009;W. ...
... White et al., 1958). Les acides minoritaires comme l'acide formique, -acétique, -citrique, -lactique, -maléique,malique, -oxalique, -pyroglutamique et -succinique (Mijanur Rahman et al., 2014) ainsi que des ions inorganiques comme l'ion phosphate et l'ion sulfate participent également à l'acidité du miel (Terrab et al., 2002;White et al., 1962). Leurs concentrations varient selon l'origine botanique et la période de récolte des miels (Barbier et al., 1961;Silva et al., 2009). ...
La présente étude a pour objectif principal de caractériser la composition chimique et pollinique des miels de Guyane afin d’ydéceler des marqueurs permettant de justifier la provenance du produit. Des spectres polliniques ont été établis et les fractions volatiles des miels ont été piégées par HS-SPME. Le dosage des composés phénoliques etla mesure de l’activité antioxydants des échantillons ont aussi été réalisés.L’étude des grains de pollens montre une importante diversité pollinique. Elle s’explique par la présence significative d’espècesspontanées et d’un climat favorisant les floraisons multiples. Les principaux taxons du répertoire guyanais ainsi que les potentiels marqueurs botaniques de la spécificité régionale ont été répertoriés. Cette étude permet à la Guyane de disposer d’une première banque de pollens apicole. Une première proposition de l’origine botanique des miels de Guyane a été formulée.L’étude de la fraction volatile des miels montre une composition principalement dominée par des composés non terpéniques oxygénés suivi par les monoterpènes oxygénés. L’analyse statistique des données positionne les 87 échantillons de miels dans 4 groupes chimiques. Enfin, les résultats du dosage des composés phénoliques ainsi que ceux de l’activité antioxydante des miels semble montrer, au premier abord, la présence de composés phénoliques. Ces données ouvrent la perspective d’une étude de ces molécules d’intérêt biologique dans les miels de Guyane.
... All kinds of honey contain these bioactive compounds but in varying concentrations. Various colorimetric assays reveal that the total phenolic content in various types of honey varies from 86 mg/kg to 1141 mg/kg [87], whereas the range for the flavonoid content is from 36 mg/kg to 150 mg/kg of honey [88]. Both flavonoids and polyphenols protect neurons against oxidative damage, improve neuronal function and enhance regeneration, protect neurons from neurotoxicity, and modulate neuronal signaling pathways [24]. ...
... The most common flavonoids and polyphenols present in almost all types of honey that are found to be beneficial against neurodegenerative diseases include apigenin, benzoic acid, caffeic acid, catechin, chlorogenic acid, chrysin, cinnamic acid, coumaric acid, ellagic acid, ferulic acids, galangin, gallic acid, hesperetin, isorhamnetin, kaempferol, luteolin, myricetin, naringenin, quercetin, and syringic acid [88] (Figure 1). Though plenty of research is available in the literature archive advocating the potential role of honey in ameliorating neurological disorders, the polyphenols components of honey proclaim way more potential roles of sweet nectar. ...
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Honey is the principal premier product of beekeeping familiar to Homo for centuries. In every geological era and culture, evidence can be traced to the potential usefulness of honey in several ailments. With the advent of recent scientific approaches, honey has been proclaimed as a potent complementary and alternative medicine for the management and treatment of several maladies including various neurological disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis, etc. In the literature archive, oxidative stress and the deprivation of antioxidants are believed to be the paramount cause of many of these neuropathies. Since different types of honey are abundant with certain antioxidants, primarily in the form of diverse polyphenols, honey is undoubtedly a strong pharmaceutic candidate against multiple neurological diseases. In this review, we have indexed and comprehended the involved mechanisms of various constituent polyphenols including different phenolic acids, flavonoids, and other phytochemicals that manifest multiple antioxidant effects in various neurological disorders. All these mechanistic interpretations of the nutritious components of honey explain and justify the potential recommendation of sweet nectar in ameliorating the burden of neurological disorders that have significantly increased across the world in the last few decades.
... As much as we know, the inhibition action of honey on PPE has not been analysed before. However, silicone analysis showed the effectiveness of twelve components of honey to human elastase heterophils demonstrating their capacity to suppress elastase [66]. It is therefore highly advised that future research investigating the behaviour of anti-elastase in many honey samples from various botanical regions at concentrations more than that examined in the current study are recommended. ...
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This research was aimed to investigate and evaluate the phytochemical, physicochemical, sensory, microbiological and pharmacological properties such as antioxidant, anticancer, anti elastase, anti-melanogenic and anti-tyrosinase activity in connection with health, safety, food and nutritional benefits of raw (RHs) and regular (ReHs) Nigerian honey. Eighteen raw honey (RHs) samples and twelve regular honey (ReHs) samples were collected from the Republic of Nigeria. Tannin content, total phenolic content, total flavonoid content, moisture, ash, pH, EC, free acidity, proline, diastase, HMF, invertase, glucose, fructose, and sucrose were the tested phytochemical and physicochemical parameters. Fiehe, Lund and Lugol qualitative test were performed to test the purity of honey samples. The results obtained from the research showed that the quality of honey samples studied were within the recommended standard (Codex). The existence of the research findings showed that RHs proved exceptional pharmacological (anticancer, antibacterial, anti-melanogenic and antioxidant) activities against the cell line (MCF-7). The highest microbial count was observed in RHs (5.5 × 0.47 × 102 cfu/100 g). There were no observable coliform growths in the samples. The findings in this current study showed that honey samples contain better consumable quality. In conclusion, honey can be potentially used as alternative treatments for controlling infectious diseases.
... Moreover, previous studies on animals reported that intake of honey was beneficial and improved memory loss and cognitive decline caused by different conditions, such as aging, stress, ovariectomy [40][41][42] and neuroinflammation induced by Aβ-42 injection [43]. The beneficial effects of honey on the brain have been associated with the presence of components such as flavonoids and phenolic acids that can improve oxidative stress and oxidative stress-linked effects [17,44,45]. ...
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The purpose of the present study was to evaluate the impact of long-term honey ingestion on metabolic disorders and neurodegeneration in mice fed a high-fat diet (HFD). Three groups of mice were fed with a standard diet (STD), HFD or HFD supplemented with honey (HFD-H) for 16 weeks. Biochemical, histological, Western blotting, RT-PCR and Profiler PCR array were performed to assess metabolic parameters, peripheral and central insulin resistance and neurodegeneration. Daily honey intake prevented the HFD-induced glucose dysmetabolism. In fact, it reduced plasma fasting glucose, insulin and leptin concentrations and increased adiponectin levels. It improved glucose tolerance, insulin sensitivity and HOMA index without affecting plasma lipid concentration. HFD mice showed a significantly higher number of apoptotic nuclei in the superficial and deep cerebral cortex, upregulation of Fas-L, Bim and P27 (neuronal pro-apoptotic markers) and downregulation of Bcl-2 and BDNF (anti-apoptotic factors) in comparison with STD- and HFD-H mice, providing evidence for honey neuroprotective effects. PCR-array analysis showed that long-term honey intake increased the expression of genes involved in insulin sensitivity and decreased genes involved in neuroinflammation or lipogenesis, suggesting improvement of central insulin resistance. The expressions of p-AKT and p-GSK3 in HFD-H mice, which were decreased and increased, respectively, in HFD mouse brain, index of central insulin resistance, were similar to STD animals supporting the ability of regular honey intake to protect brain neurons from insulin resistance. In conclusion, the present results provide evidence for the beneficial preventative impact of regular honey ingestion on neuronal damage caused by HFD.
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Obesity is a metabolic disorder that has become critically prevalent throughout the world. Obesity has been linked to other chronic diseases such as diabetes mellitus, cardiovascular diseases and cancer. Natural products such as honey have been investigated for their potential effect on obesity. Hence, this study systematically reviewed the recent literature concerning the effects of honey on obesity in obese animal models and in people with obesity. The Ovid MEDLINE, PubMed, Scopus, Web of Science and Google Scholar electronic databases were searched for relevant articles. A total of 130 relevant articles were obtained from the initial search. Following a thorough screening, nine articles were selected for data extraction, including six animal studies and three clinical trials. In most of the animal studies, honey demonstrated an anti-obesity effect by reducing body weight, body fat composition and adipocyte size, among others. However, supplementation of honey in clinical trials showed conflicting results. Even though honey supplementation did not demonstrate any weight-reducing effect in some of the clinical trials, none of the trials showed that honey increases body weight. However, the results should be interpreted with caution as most of the studies involved animal models and there is a limited number of high quality, randomized, controlled clinical trials. Systematic Review Registration PROSPERO, identifier 10.37766/inplasy2022.6.0038.
A multivitamin is a medication intended to serve as a salutary supplement with vitamins, salutary minerals, and other nutritive rudiments. Multivitamin formula contain vit C, B2, Zinc, Calcium, Magnesium, Potassium. gummy vitamins are designed to be a further palatable( read sweeter) volition to regular vitamins in the expedients that people will be more inclined to take them. numerous people prefer sticky vitamins to capsules due to their gooey flavours and delicacy- suchlike taste. Dissolvable, chewable, greasepaint or sticky vitamins tend to be easier to digest. Like capsules and capsules, gummies supply the vitamins. Vitamin C and Vitamin B2( riboflavin) are the idol constituents of multivitamin gummies, both gives the antioxidant exertion, Photoprotection, crack mending, ameliorate hair growth and remedial uses on eye related conditions, migraine and exertion on healthy skin/ hair independently. Citric acid have defensive goods in the body. It's used in sticky, can kill bacteria and lower the acid in urine. Agar is extensively used as gelling, thickening, stabilizing and density controlling agent for gummies. Pure honey is a enhancing agent that makes gummies delicious to eat. Orange juice shows antioxidant exertion and gives delicious flavour to sticky.
Conference Paper
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Milk is often contaminated with many toxins, with aflatoxins being the most prominent of them. Aflatoxin M1 (AFM1) is a toxin of high risk in milk, due to its carcinogenicity, mutagenicity, teratogenicity and immunosuppressive effects on humans. The worldwide occurrence and prevalence of aflatoxins in milk products has raised the need for strict legislation to regulate these toxins at safe levels for human consumption. The carryover of aflatoxin B1 from feed to aflatoxin M1 in milk is a great concern for vulnerable age groups such as infants and the elderly. Currently, the European Union and the US Food and Drug Administration have set legal limits for the presence of aflatoxins in dairy products. Nevertheless, the incidence of aflatoxins in milk and milk products is reported in levels higher than the regulatory limits. This paper reviews some of the analytical methods used to detect aflatoxins and various strategies for the control and decontamination of aflatoxins in milk products.
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Depression also known as clinical depression, is a mental disorder of public health concern that should be properly and immediately treated because a poor medical follow up can lead to suicide resulting to death or major body self-infliction of harm. Prediction of the phytochemical compounds in honey on neurotransmitters and enzymes involved in depression were investigated by in-silico studies. This research was done to create docking scores, predict pharmacodynamics of honey and to identify the potential oral drugs used for the treatment of depression Studies have shown that honey and related by products like propolisto be very useful in the treatment of depression. In this preclinical research, animal models was used to demonstrate the antidepressant effect of honey on female albino mice. These tests included tail suspension test and forced swim test, during which they were shared into four groups. From the results obtained honey showed a promising antidepressant activity together with a better synergism with imipramine. From the molecular docking scores obtained, honey was found to have phytochemical compounds (examples) with good potentials to be oral antidepressants especially Chlorogenic acid.
Headspace solid-phase microextraction (SPME) with an 85 μm Carboxen polydimethylsiloxane (CAR/PDMS) fiber was used to extract volatile compounds, and a gas chromatograph equipped with a mass spectometry detector (GCMS) was used to identify the volatile compounds in honeys. Thirty-four different volatile compounds from the headspace of honey produced in the central valley of Ñuble Province, Chile, were extracted with fiber coating CAR/PDMS. The identified compounds were: 10 alcohols, 9 acids, 6 ketones, 3 aldehydes, 2 furans, 2 terpenes and 2 lactones. Only four of the volatile compounds had never been reported before as honey compounds; these being: 1,3-propanodiol, 2-methyl butanoic acid, 3,4-dimethyl-3-hexen-2-one, and 6-methyl-5-octen-2-one. These four compounds were found in three of the 10 analyzed samples. The compounds found in the highest percentage of area were ethanol, acetic acid, 1-hydroxy-2-propane, 3-hydroxy-2-butane, and furfural. However, the analyzed samples did not present a distinctive profile.
From ancient times, honey was not only used as a natural sweetener but also as a healing agent. Many health-promoting and curative properties attributed to it are the basis for some traditional folk medicine treatments throughout the world today. Its beneficial effects in different disorders, rediscovered in recent decades, varying from its antibacterial effects and benefits in wound healing to its safe role in peptic ulcer, gastroenteritis, oncology, ophthalmology, dermatology and dental hygiene. This will be discussed in this review on the basis of a series of scientific studies conducted to investigate the therapeutic properties of this natural product.
Publisher Summary Honey is regarded as the nectar and saccharine exudation of plants, gathered, modified and stored in the comb by honey bees. It is levorotatory and contains not more than 25% water, 0.25% ash, and 8% sucrose. Initially, honey was considered to be a mixture of D-glucose, D-fructose, and sucrose. The presence of maltose in some honeys was also recognized. A large-scale fractionation was undertaken by Siddiqui and Furgala on a carbon-Celite column. They used an enriched oligosaccharide fraction, isolated from honey by using a batch operation employing carbon-Celite as the adsorbent. The fractions eluted with 2.5–15% aqueous ethanol were further separated by paper chromatography, occasionally by paper electrophoresis and frequently by thin-layer chromatography after acetylation. These fractionation procedures resulted in the characterization of at least 24 oligosaccharides. It has been observed that in the formation of these saccharides, both trans-D-glucosylation and trans-D-fructosylation occurs. In the former process, D-glucopyranosyl groups are transferred from a D-glucopyranosyl donor to an acceptor molecule. In the latter process, D-fructofuranosyl groups are transferred by a D-fructofuranosyl-transferring enzyme to other sugars.
The disaccharides maltose, kojibiose, isomaltose, nigerose, neotrehalose, gentiobiose and laminaribiose were isolated from honey and characterized as crystalline octaacetates. Sucrose and turanose were obtained in the crystalline form and maltulose as the crystalline osazone. Isomaltulose and 1-α-glucosylfructose were tentatively identified. The approximate proportions of these sugars in the oligosaccharide fraction (3·65%) of the honey have been calculated, as follows: maltose, 29·4%; kojibiose, 8·2%; turanose, 4·7%; isomaltose, 4·4%; sucrose, 3·9%; ketose band (mixture of at least three ketoses including maltulose and isomaltulose), 3·1%; nigerose, 1·7%; neotrehalose, 1·1%; gentiobiose, 0·4% and laminaribiose, 0·09%.
The Rasayan branch of Ayurveda deals specifically with and Rasayan formulations bestows upon the user, the longevity, with age stabilization, retaining youth for longer with maintaining strength of all organs optimally, enhanced intelligence, aphrodisiac prowess, improved complexion, voice and allied positive health attributes. Presently considerable research is being carried out on various Rasayan Products and the herbs to screen them for various therapeutic benefits. But the research is focusing only one or couple of aspects of Rasayan's therapeutic benefits. The exhaustive research on all therapeutic benefits of single Rasayan product will be more conclusive validation of claims of classical Ayurvedic texts. This perspective review also details main Rasayan formulations with emphasis on the herbs used in them, so that we could direct our focus of research on them and that too exhaustively.
Volatile organic compounds in honey are derived from numerous biosynthetic pathways and contribute in the organoleptic and aromatic properties of honey as well as aid in its floral and geographical origin determination. They are usually extracted from the sugar matrix using various methods associated with varying degree of selectivity and effectiveness. In this study, the volatile composition of three local South African honeys was explored by solvent extraction and identified by a gas chromatograph equipped with a mass spectrometry detector. Thirty-two volatile compounds were identified and classified as hydrocarbons (3), acids (3), aldehydes (3), ketones (3), benzene derivatives (4), terpenes and its derivatives (3), alcohols (6), furans (2) and pyran (1) derivatives and others (4). The compounds found in the relatively highest percentage of area were hexane, methanamine hydrochloride, butanal and acetic acid. Astoundingly, thiophene and N-methyl-D3-Aziridine, essential precursors used for the synthesis of natural products and pharmaceuticals with vital biomedical properties, plus methanamine hydrochloride were the additional compounds identified in these honeys. However, the botanical identification of a honey is based on plant-derived metabolites such as norisoprenoids, terpenes, benzene compounds and their derivatives. Further studies are needed to characterize the aroma constituents as well as to determine the botanical and geographical origins of these honeys in a bid to standardize their quality, to avoid fraud and to authenticate them.