Phtopharmacology of Tulsi-Basil (Ocimum sanctum) Part 4
Phtopharmacology of Tulsi-Basil (Ocimum sanctum) Part 4
Properties and Pharmacology
Ayurvedic
Properties
Rasa: Katu (Acrid, Pungent), Tikta (Bitter), Kashay
(Astringent)
Weerya: Ushna (Hot)
Wipaka: Katu (Acrid, Pungent)
Guna: Ruksha (Dry
or Drying), Laghu (Light)
Ayurvedic
Actions (Karma):
Deepana: Appetizer, Relieves anorexia
Ruchya: Imparts taste, Improves taste
Hridya: Cardiac tonic, Beneficial to heart
Waatahara: Improves neuromuscular functions, Relieves neuralgia,
Relieves arthralgia,
Pittahara: Antihistaminic
Kaphahara: Reduced expectoration
Durgandhihara:
Relieves various types of foul smells
[80]
Krumidoshahara:
Anthelmintic [81]
Teekshna: Penetrating
Daahawardhinee: Increases burning sensation
Pittawardhinee: Cholagogue
Agniwardhinee: Improves appetite and digestion
Shwaasahara: Relieves breathlessness, Bronchitis,
Bronchial asthma
Hidhma (Hikkaa) Shaamaaka: Relieves hiccup (Hiccough)
Vami (Chhardi) jit/ Vamihara : Relieves vomiting
Krumijit: Anthelmintic
Jwarahara: Antipyretic
Mootrakricchra: Burning micturition
Ashmaree: Urinary stones
Netraroga: Ophthalmic disorders
Vishghna: Antitoxic
[82]
Pratishyaayghna: Relieves common cold (? Nasal allergy)
Wranashodhana: Useful
for the treatment of wounds and ulcers
Paarshwaruk:
Relieves backache, Relieves flank
pains (? Renal colic)
Kushthajit/Kushthahara:
Relieves skin diseases, (? Leprosy)
Wishajit/Wishhara: Anti-toxic
Krucchrajit: Useful
for burning micturition [83]
Shanti krut: Imparts (mental) peace
Druk-krut: Beneficial
for vision
Bhootahara: Useful
in psychiatric illnesses [84]
Ayurvedic Ganas/Warga
Charaka Samhita: Shwasahara gana
Shrushut Samhita: Surasaadi gana
Ashtaang Hridaya: Surasaadi gana and Kaphaghna gana
Ashtaang Sangraha: Surasaadi gana and Shwaasahara gana
Bhaawapraakash Nighantu: Pushpa Warga
Raajanighantu: Karaweeraadi Gana
Dhanwantari Nighantu: Karaweeraadi Gana
Madaanapaala Nighantu: Karpooraadi warga
Kaiyadeva Nighantu: Oushadhi Warga
Shodala Nighantu: Karaweeraadi Gana
Priya Nighantu: Shatapushpaadi warga
Haritakyaadi Nighantu: Pushpa Warga
Shaligraam Nighantu: Pushpa Warga
Nighantu Aadarha: Tulsyaadi Warga [85]
Modern View
Eugenol
Molecular
formula: C10H12O
Structural
formula:
Eugenol is an allyl chain-substituted guiacol. Eugenol
is a colorless to pale yellow, aromatic oily liquid. Apart from Tulsi-Holy
basil (Ocimum tenuiflorum), in nature
it occurs in clove, nutmeg, cinnamon, bay leaf etc. Eugenol has a pleasant,
spicy clove-like scent. Eugenol possesses anti-inflammatory, antioxidant,
antimicrobial, antiviral, antifungal, analgesic and antitumor properties. [86]
In dentistry eugenol is very frequently used as a
temporary dressing during dental filling and in root canal therapy.
Zinc oxide eugenol, pseudoisoeugenol, Methyl eugenol
and isoeugenol are the compounds of eugenol available in market.
Oxidative stress and inflammation are partners in many
pathological processes. During oxidative stress there is excessive production
of reactive oxygen species (ROS) that sets in motion the inflammatory process
which damages the body systems. Antioxidant activity of eugenol effectively
suppresses the resulting inflammations and prevents tissue damage.
Pan and Dong demonstrated that eugenol inhibited the
ovalbumin induced eosinophilia in the lung tissues. This data suggests that
eugenol can be a therapeutic agent in the treatment of inflammatory lung
diseases such as bronchitis, pneumonia and bronchial asthma.
The diesel particles induce airspace collapse and
alter pulmonary mechanics. The pneumotachography (a quantitative measure of
airflow volume) in animal models showed that eugenol reduced the inflammation
and pulmonary damage caused by diesel exhaust particles. The data demonstrated
that eugenol can be a potent agent to treat the damage caused by air
pollution.
Eugenol was also found to be useful in cardiac
remodeling following myocardial infarction. Further anti-inflammatory and
antithrombotic properties of eugenol were effective in preventing myocardial
ischemia.
Anti-inflammatory property of eugenol ameliorated the
structural and functional liver damage caused by hepato-toxic agents.
Using cell culture pre-exposed to a receptor activator
of NF-κB ligand (RANKL) Deepak et al demonstrated that eugenol prevented the
osteoclast differentiation in a dose dependent manner. A recent study
demonstrated that administration of eugenol for twelve weeks attenuated the
alveolar bone loss and remodeling associated with estrogen insufficiency in
ovariectomized rats.
A study showed that anti-inflammatory property of
eugenol exerted antitumor effect. A recent study showed that eugenol promoted
cytotoxicity against breast cancer cells. Additionally, a recent study reported
that eugenol also exerted synergistic chemotherapeutic effects with cisplatin.
[87]
Well! All is not so rosy with the actions of eugenol.
In perfume industry some people may become sensitized to eugenol. The degree to
which eugenol can cause an allergic reaction in humans is disputed. When
eugenol is used in dental preparations such as tooth pastes or dental packing
and dental cement it may cause contact stomatitis and allergic cheilitis. [88]
Toxicity
Eugenol may cause nausea, diarrhea,
tachycardia, dizziness, convulsions and unconsciousness. Eugenol is
hepatotoxic. Eugenol can cause dental pulp fibrosis. In mice eugenol could
cause genotoxicity by inducing DNA damage. [89]
Rosmarinic
acid
Molecular
formula: C18H16O8
Structural
formula:
[90]
Rosamarinic acid is a phenolic compound
and ester of caffeic acid. Rosamarinic acid occurs naturally in several plants
of Lamiaceae family from which it was
originally isolated.
Rosamarinic acid has anti-inflammatory
property which protects neurons against oxygen-glucose deprivation. Treatment
of rats five hours after ischemia-reperfusion reduces brain infarct.
Rosamarinic acid displays
immunomodulatory activity
Rosamarinic acid increases the melanin
content and tyrosinase expression in melanoma cells. [91]
Rosamarinic acid (RA) suppresses amyloid β (A β)
accumulation in mice thus preventing the development of Alzheimer’s disease.
[92]
Rosamarinic acid reduces inflammations and various
allergic conditions
Rosamarinic acid is a novel agent useful in the treatment
of autoimmune diseases [93]
Apigenin
Molecular
formula: C15H10O5
Structural
formula:
Apigenin is a naturally occurring flavones found in
many plants. Apigenin is particularly abundant in the flowers of chamolile
plants. It is a yellow crystalline solid. [94]
Apigenin is insoluble in water but is soluble organic
solvents. Delayed plasma clearance and slow decomposition in liver increases
its bioavailability. It is potent anti-inflammatory and anti-toxicant agent. It
is useful in the treatment of rheumatoid arthritis, various autoimmune
disorders, Parkinson’s disease, Alzheimer’s disease and various types of
cancers.
Research has shown that apigenin has strong
antimicrobial, antiviral, antifungal and antiparasitic activities. It is bactericidal
for human gut bacteria.
Apigenin is ineffective against Staphylococci. However it protects lung cells against aureus pneumonia. Apigenin also protects
human basal alveolar cells against adenocarcinoma.
Streptococcus
mutans is the main pathogen responsible
for the development of dental caries in humans. Apigenin can inhibit this
organism and prevent dental caries.
Apigenin kills many antibiotic resistant bacteria.
Some derivatives of apigenin showed antibacterial activity against Staphylococcus aureus, Bacillus subtilis,
Escherichia coli and Pseudomonas aeruginosa. Apigenin or its derivatives
could be candidates as new antibacterial agents. Like rifampicin, apigenin
targets RNA polymerase and gyrase, and like norfloxacin targets DNA
topoisomerase IV.
At the dose 60mg/kg body weight apigenin significantly
decreases colonization of Helicobactor
pylori in the pyloric antrum and neutrophil and monocyte infiltrations.
Apigenin also protects the stomach from atrophic gastritis.
Synergy has been observed between apigenin many other
antibiotics.
Synergy has been observed
between apigenin and other antibiotics
Apigenin inhibits multiple viruses e.g. enterovirus 71
(EV71), herpes simplex virus HSV-1 and
HSV-2, hepatitis C virus, influenza virus and African swine fever virus (ASFV),
but not coxsackievirus A16 (CAV16). By interfering with viral internal ribosome
entry site (IRES), apigenin exerts its antiviral action.
Apigenin was found to inhibit Hepatitis C virus (HCV)
replication in vitro. Therefore,
apigenin intake, either through regular diet or supplements, may be beneficial
for chronically infected patients.
Apigenin exerts antifungal activity against Candida albicans ATCC10231 and Candida parapsolis ATCC 22019. Apigenin
can be used as an antifungal agent in the treatment dermatophytosis. A recent
study revealed that apigenin altered the cell membrane potential, increased
cell permeability and induced membrane dysfunction in pathogenic fungi.
Apigenin treatment for 24 hours resulted in inhibition
of parasite causing Leishmaniasis. This effect is due to antioxidant activity
of apigenin. In addition apigenin induces extensive swelling in the
mitochondria of the parasite, alters mitochondrial membrane potential, ruptures
Golgi network and causes cytoplasmic vacuolization.
Oral consumption of apigenin is safe. [95]
Myrtenal
Molecular
formula: C10H14O
Structural
formula:
Myrtenal also known as fema 3395 belongs
to the class of organic compounds known as bicyclic monoterpenoids. Apart from
Tulsi-Basil (Ocimum tenuiflorum)
Myrtenal is found in cardamom, pepper, thyme, ginger, orange, lemon and other
plant oils. Myrtenal is very hydrophobic, insoluble in water. Myrtenal has
anti-inflammatory and antioxidant properties.
[96]
Luteolin
Molecular
formula: C15 H 10 O6
Structural
formula:
Luteolin is a crystalline flavone.
Luteolin was first isolated in pure form and named in 1829 by the French
chemist Michel Eugene Chevreul. The empirical formula of luteolin was
determined by the Austrian chemists in 1864 by Heinrich Hlasiwetz and Leopold
Pfaundler. In 1896 luteolin’s correct structural formula was proposed by the
English chemist Arthur George Perkin.
Luteolin is a yellow dye found in
leaves, barks, rinds and pollens of aromatic flowering plants. Dietary sources
include celery, broccoli, parsley, thyme, green pepper, tea, carrots,
peppermint and navel oranges. [97]
Pharmacokinetics
of Luteolin
After a single bolus dose of 50mg/kg body weight
administered intravenously the half life was found to be 8.94 hours for
unconjugated (free) and 4.98 hours for conjugated luteolin. Following oral
administration, the plasma concentration of luteolin attained the maximum level
5.5μg/mL at 5 minutes and decreased to below100 ng/mL after 1 hour. The low
bioavailability (4.10%) of luteolin after oral administration was said to be
due to significant first pass effect. After intravenous (IV) administration the
maximum concentration of luteolin in the plasma was 23.4μg/mL at 0 hour.
Luteolin was found to have a large volume of distribution and high clearance.
Double peaks found after oral and intravenous administration suggest
enterohepatic recirculation. [98]
Uridine 5’-diphospho-glucuronosyltransferase is a
microsomal glycosyltransferase that catalyses the transfer of the glucuronic
acid component of UDP-glucuronic acid to small hydrophobic molecule. Luteolin
partially exerts its biologic effects via its metabolites catalyzed by
UDP-glucoronosyltransferases (UGTs) and catechol-O-methyltransferases
(COMTs)
Anti-inflammatory property of
Luteolin
Luteolin inhibits TNF-α, IL-6, iNOS
and COX-2 gene expression responsible for inflammation. Luteolin also reduces
DNA binding activity of nuclear factor-kappaB (NF-κB) in lipopolysacchaeide
(LPS)-activated macrophages. Luteolin also inhibits the generation of reactive
oxygen species. These observations suggest that luteolin is a potent
anti-inflammatory agent and can be useful for treating pulmonary inflammatory
disorders. [99]
Allergic inflammation and autoimmune
diseases such as dermatitis, psoriasis and multiple sclerosis (MS) involve
activation of T-cells and mast cells. Luteolin inhibits activation of T-cells
and mast cells to control allergic inflammation and autoimmune diseases. [100]
Luteolin displays specific
anti-inflammatory effects at micromolar concentrations which are partly due to
its antioxidant property. Its major anti-inflammatory effects are attributed to
activation of antioxidative enzymes, suppression of NFκB pathway and inhibition
of pro-inflammatory substances. After oral or intravenous administration, in vivo, luteolin also reduces the
increased vascular permeability in inflammations. Epidemiological studies show
that luteolin has the potential to prevent diseases associated with
inflammatory processes especially some cardiovascular diseases. [101]
Anti-allergic
activity of luteolin
In animal studies, like quercetin,
baicalein and prednisolone, luteolin inhibited IgE antibodies and suppressed
allergic reactions. In a study in mice luteolin inhibited the IgE
antibody-mediated biphasic cutaneous reaction (immediate phase reaction and
late phase reaction). In a study in rats, luteolin inhibited IgE-mediated
histamine release from bone marrow and peritoneal mast cells. Luteolin also
inhibited IgE-mediated TNF-α and IL-6 production from bone marrow-derived
cultured murine mast cells (BMMC=bone marrow-derived mast cells). However,
luteolin did not affect histamine-, serotonin- and platelet activating
factor-induced cutaneous factors in rats.
[102]
Immunomodulatory
activity of Luteolin
The production of hemolysin in mice,
experimental allergic encephalitis in guinea pigs and the proliferative
response of mouse splenic lymphocytes in
vitro suggest that luteolin has a potent immunostimulatory property. This
also suggests that luteolin can be effective in the treatment of chronic
bronchitis. [103]
Actions of Luteolin on the skin
Sustained release niacin effectively
lowers serum cholesterol, lowdensity lipoprotein (LDL) and triglycerides while
raising high density lipoprotein (HDL). However 75% of patients experience
cutaneous warmth and itching due to flush. Through decreasing prostaglandin
acetyl salicylic acid reduces flush by 30%. However luteolin decreases
prostaglandin D2 (PG D2) and 5-hydroxytryptamine (5-HT) and
decreases niacin-induced flush. [104]
The pathogenesis of the
depigmentation disorder vitiligo (in commonman’s words leucoderma) is yet
unclear. Interlukin-8 (IL-8) is a key inflammatory chemokine. In vitiligo IL-8
gene expression from melanocytes is significantly increased. By suppressing this
gene expression from melanocytes, luteolin significantly controls the
development of vitiligo. This suggests that luteolin can be useful for the
treatment of vitiligo. [105]
Actions of Luteolin on Mouth
Periodontal disease comprises of a
group of infections that lead to gingivitis, periodontal tissue distruction and
alveolar bone loss with tooth exfoliation. The Gram-negative organism Actinobacillus actinomycetemcomitans which
possesses and produces lipopolysaccharide (LPS) molecules play a key role in
disease development. Pretreatment with luteolin abolishes the
lipopolysaccharide (LPS) effects on NF-κB translocation. These effects are
attributed to the anti-inflammatory and antioxidant properties of luteolin. It
is said that luteolin interferes with lipopolysaccharide (LPS) signaling
pathways, reducing activation of several mitogen-activated protein kinase
family members and inhibits inflammatory mediator expression. [106]
Actions of Luteolin on Hematopoetic System
Luteolin has apoptosis inducing
ability against human leukemia (HL-60) cells. By decreasing the mitochondrial
membrane potential, luteolin induces apoptosis in human leukemia (HL-60) cells.
[107]
Anti-degenerative activity of Luteolin
By virtue of its antioxidant,
anti-glycative and anti-degenerative properties, luteolin exhibits antiaging
property. [108]
Actions of Luteolin on behavior
Autism spectrum disorder (ASD) is a
condition defined by social communication deficits and repetitive restrictive
behaviors. Autism usually develops within first three years of life. The
diagnostic criteria for autism spectrum disorder (ASD) are as follows:
1. Deficits in social interaction and
communication across various contexts;
2. Restricted, repetitive patterns of
behavior, interests or activities;
3. Symptoms must be existing since
early childhood
4. Clinically symptos cause
impairment in social or occupational functioning
5. These disturbances are not
explained by intellectual disability
A study showed treatment with
luteolin ameliorated social and nonsocial behaviors [109], [110]
Many neurological disorders
accompanied by cognitive deficits exhibit abnormal synaptic function. This
emerging concept is exemplified by Alzheimer’s disease. Alzheimer’s disease
begins with subtle alterations in hippocampal synaptic efficacy prior to frank
neuronal degeneration. A study on rats showed that luteolin could enhance
synaptic transmition in dental gyrus of hippocampus. Chronic cerebral hypoperfusion
was also shown to impair special learning and memory. Treatment with luteolin
reversed the learning and memory deficit. [111]
Actions of Luteolin on Nervous system
Modulating the A type γ-aminobutyric
acid receptors (GABAAR) is one of the major drug targets for
neurological and psychological diseases. By modulating the A type
γ-aminobutyric acid receptors (GABAAR) luteolin shows
antidepressant, antinociceptive and anxiolytic effects. [112]
By reducing oxidative stress luteolin was found to be effective
in the treatment of epilepsy. [113]
Luteolin relieves neuropathic pain via GABAA receptor
and opioid receptor [114]
In a study on mice, luteolin showed anticancer effect
in Neuro-2a neuroblastoma cells. By inducing accumulation of reactive oxygen
species in cancer cells, luteolin induced cell death in Neuro-2a neuroblastoma
cells. Some researchers showed that luteolin induced apoptosis in neuroblastoma
cells through endoplasmic reticulum stress and mitochondrial dysfunction. [115]
Actions of
Luteolin on Respiratory System
By changing the expression of apoptotic markers, such
as caspase-3 and caspase-independent protein expression luteolin at a dose 50μM
induces apoptosis in lung carcinoma CH27 cells. Luteolin shows damaging effect
on DNA. Luteolin also induces S-phase cell cycle arrest. Thus luteolin kills
CH27- lung cancer cells by its caspase-dependent and caspase-independent
pathway. [116]
Hexavalent chromium [Cr(VI)] is a well-known
carcinogen associated with human lung cancer. By virtue of its antioxidant and
anti-inflammatory properties, luteolin significantly inhibits chromium induced
cancer. [117]
Non-small cell lung cancer is the commonest lung
cancer. A study showed that luteolin exerts significant anti-tumor effect on
erlotinib-resistent non-small cell lung cancer cells at cellular levels. [118]
Actions of
Luteolin on Cardiovascular System
Recent scientific literature has reported
cardio-protective action of luteolin. Luteolin protects myocardium from
ischemia-reperfusion injury, heart failure and ill effects of atherosclerosis.
These activities are attributed to anti-inflammatory and antioxidative
properties of luteolin. [119]
A recent study on rats showed that luteolin protects
the myocardium from ischemia re-perfusin injury. Further, luteolin improved the
shortening of cardiomyocytes from ischemia and prevented the apoptosis. [120]
The migration and proliferation of vascular smooth
muscle cells (VSMAs) are the critical pathological processes in cardiovascular
diseases especially associated with atherosclerosis. By its antioxidant
property, luteolin inhibits the proliferation of vascular smooth muscle cells
(VSMAs) and retards the development of atherosclerosis. [121]
Another study on rat aorta showed that depending upon
the concentration used, luteolin inhibited platelet-derived growth factor
(PDGF)-BB-proliferaion of vascular smooth muscle cells (VSMAs) to evoke
relaxation of aorta. [122]
In a study on isolated aorta of Sprague-Dawly rats,
luteolin via its action on vascular endothelium evoked the relaxation of the
vessel. In the study phenylephrine was used to induce vasoconstriction. The
aorta was then treated with luteolin. Depending upon the dose used luteolin
evoked vasorelaxation. [123]
A study on the thoracic aorta
of rat showed that luteolin was potent calcium (Ca2+)
channel blocking agent. The release of intracellular calcium (Ca2+)
and activation of potassium (K+) channel was also observed. All
these factors were responsible to bring about vasodilatation. Further it was
found that α and β-adrenoceptors were not involved in its relaxation. [124]
Ischemia-reperfusion injury is associated with
activation of Caspase 3 in cardiomyocytes. Caspase 3 is responsible for
shortening and apoptosis of cardiomyocytes. A study on Sprague-Dawley rats
demonstrated that luteolin inhibited the activation of Caspase 3, protected the
cardiomyocytes and prevented their necrosis and apoptosis. Luteolin also
improved the contractile function of cardiomyocytes following
ischemia-reperfusion injury. [125]
By using semi-synthetic active component of luteolin,
researchers were able to lower elevated blood pressure. Injection of
semi-synthetic luteolin either intothe common carotid artery or in the fourth
ventricle of the brain lowered the blood pressure. This suggests that the
action of luteolin is central. Further, by using inderal the effect of luteolin
was weakened. This suggested that luteolin is related to exciting β-receptor.
Pituitrin raises blood pressure. Luteolin antagonizes this effect of pituitrin.
Therefore researchers conclude that luteolin can dilate blood vessels
directly. [126]
Actions of
Luteolin on the Liver
Administration of acetaminophen at high doses elevates
serum levels of pro-inflammatory factors such as inducible nitric oxide synthase
(i-NOS), tumor necrosis factor (TNF)-α, nuclear factor kappa B (NF-κB) and
interleukin-6 (IL-6). By depressing the expression of pro-inflammatory factors,
luteolin protects the liver against acetaminophen-induced liver toxicity.
Moreover, luteolin down-regulates acetaminophen-induced nitrotyrosine (NT)
formation and endoplasmic reticulum (ER) stress. [127]
In a study luteolin induced cytosolic release of
cytochrome c and activated Cysteine
Protease CPP32. CPP32 is activated during apoptosis. By this mechanism luteolin
induced apoptosis in human hepatoma HepG2 cells. [128]
Luteolin exerts its pro-apoptotic action through
generating intracellular reactive oxygen species (ROS). This contributes to the
activation of mitochondria-mediated apoptosis in cells. In addition luteolin
induces the activation of caspase-9 and caspase-3. Thus luteolin decreases the
viability of cholangiocarcinoma (CCA) cells [129]
Midazolam is a mild, sort-acting hypnotic-sedative,
anxiolytic, anti-convulsant and muscle relaxant. Midazolam is metabolized in
the liver microsomes. Luteolin depresses midazolam metabolism. Further luteolin
may cause pharmacokinetic interactions with drugs co-administered with
midazolam. [130]
Actions of
Luteolin in metabolic disorders
Diabetes mellitus (DM) is a multimetabolic disorder.
By increasing oxidative stress, it causes dyslipidemia and cardiomyopathy.
Luteolin corrects dyslipidemia. The antioxidant property of luteolin protects
the heart from diabetic cardiomyopathy. [131]
In experimental study on animals, luteolin lowered
elevated blood sugar in streptozotocin (STZ)-induced diabetes. Further,
luteolin also lowered elevated lipids. Luteolin also normalized the blood
pressure without interfering with sugar levels. [132]
Antitumor
activity of Luteolin
The flavonoid luteolin found in
Tulsi-Basil (Ocimum tenuiflorum)
exert anti-tumor/anti-carcinogenic, anti-mutagenic, anti-proliferative effects.
These effects are attributed to anti-inflammatory and anti-oxidant properties
luteolin.
Luteolin significantly inhibits
endothelial growth factor and A431 cell proliferation.
Anti-inflammatory, antioxidant,
immunomodulatory and anti-carcinogenic mechanisms suggest that luteolin might
be a valuable agent for cancer therapy. [133]
Anti-inflammatory property of luteolin induces
apoptosis in cancer cells. Luteolin also sensitizes cancer cells to
chemotherapeutic agents. Luteolin inhibits cell proliferation, angiogenesis and
development of metastases. Luteolin could be an anticancer agent for various
cancers. Recent epidemiological studies have shown that luteolin has cancer
prevention property. [134]
β-sitosterol
Molecular
formula: C29H50O
Structural
formula:
β-Sitosterol is a phytosterol. Its
chemical structure is similar to that of cholesterol. It is a white waxy powder
with a characteristic odor. It is hydrophobic and soluble in alcohols.
β-Sitosterol is a precursor of anabolic
steroid boldenone. Boldenone is commonly used in veterinary practice to induce
growth in cattle. It is most commonly abused anabolic steroid in sports.
There is a rare autosomal recessive
genetic disorder phytosterolemia wcich causes over absorption of phytosterols. [135]
β-Sitosterol is widely distributed in
rice-bran, wheat germ, pea nuts, soya beans, vegetable oil, corn oil and
fruits.
β-Sitosterol is used to reduce benign
prostatic hyperplasia and elevated serum cholesterol. β-Sitosterol does not
appear to reduce the size of the prostate but improves urinary symptoms and
flow measures. This benefit persists for up to 18 months of use. β-Sitosterol
is used as hair supplement.
The dose of β-Sitosterol is 60 mg twice
daily. The dose can be reduced to 30 mg mg twice daily after the symptoms improve.
[136]
Uses
of β-sitosterol
Baldness: β-sitosterol helps hair growth and relieves baldness.
Burns:
β-sitosterol is useful
for treating second degree burns. Ointment containing β-sitosterol and
berberine works as well as silver sulfadiazine ointment.
Various
allergies
Psoriasis
Rheumatoid
arthritis
Fibromyalgia
Systemic
lupus erythematosus (SLE)
Chronic
fatigue syndrome
Migraine
Respiratory
disorders: β-sitosterol
is useful for the treatment of bronchitis, cough of unknown etiology,
tuberculosis and bronchial asthma
Gallstones
Prevention
of colonic cancer
Hypercholesterolemia: β-sitosterol lowers the elevated levels
of total cholesterol and LDL cholesterol but does not raise HDL cholesterol
levels.
Prostate
problems: β-sitosterol
gives symptomatic relief from benign prostatic hyperplasia. β-sitosterol does
not shrink the enlarged prostate. It is useful for the treatment of prostatic
infections. It can correct erectile dysfunction.
Cervical
cancer
Menopausal
syndrome
Other
conditions [137]
Carnosic
acid
Molecular
formula: C20H28O4
Structural
formula:
[138]
[139]
Carnosic acid is a phenolic diterpene found in
rosemary (Rosmarinus officinales).
Carnosic acid has antioxidant, anti-inflammatory antimicrobial properties.
Carnosic acid is used in tooth paste, mouth wash and chewing gum in which it
has antimicrobial effect on the microbes responsible for halitosis (fowl
smelling breath). For the same reason carnosic acid is used in skin care
products. [140]
In experimental study, anti-inflammatory property of
carnosic acid was found to protect white blood cells from developing leukemia. [141]
By inhibiting microsomal prostaglandin E2
Synthase-1, carnosic acid exhibits a potent anti-inflammatory activity. [142]
Another study showed that anti-inflammatory property
of carnosic acid is useful for treating inflammatory and infective skin
diseases and various types of arthritis. [143]
Carnosic acid shows anti-methicillin resistant
staphylococcus aaureus (anti-MRSA) activity. Carnosic acid shows synergistic or
additive effect with ampicillin and oxacillin. [144]
To investigate the chemopreventive potential of
carnosic acid on oral cancers, by painting 0.5% 7,12,-dimethylbenz(a)nthracene
(DMBA) in liquid paraffin three times a week, tumor was induced in hamster
buccal pouch. Oral administration of carnosic acid at a dose of 10mg/kg body
weight per day to (DMBA)-treated animals completely prevented the formation of
tumor in the buccal pouches of the hamsters. According to researchers, the
chemopreventive potential of carnosic acid is due to its anti-lipid
peroxidation activity. Carnosic acid also exerts modulating effect on
carcinogen detoxification enzymes during DMBA-induced oral carcinogenesis.
[145]
Oxidized lipids are hazardous to health. In vitro and
in vivo carnosic acid and carnosol are lipid protectors against lipid oxidation
and protect body systems.
Application of carnosic acid and carnosol reduce
photosensitivity and protect the skin from radiation insult. [146]
7,12-dimethylbenz[a]nthracece (DMBA) exerts
destructive effect on bone formation (clastrogenesis). Anti-oxidant property of
carnosic acid exerts anti-clastogenic effect. [147]
Carnosic acid and its derivative carnosol are are
catechol-type electrophilic compounds. Carnosic acid and carnosol exert
protective effect on neurons. They prevent glucose intolerance and obesity.
They prevent proliferation of various cancer cell lines. [148]
Arsenic is hepatotoxic. In experimental study on rats,
arsenic hepatotoxicity was induced by using 10mg/kg body weight of sodium
arsenite (NaAsO2). The rats were treated with 1-4μM carnosic acid. The
treatment exhibited increase in viability of hepatic cells. The viability was
dependent on the dose of carnosic acid. This effect was attributed to the
antioxidant property of carnosic acid. [149]
By releasing cytochrome C and apoptosis-inducing
factor (AIF) from mitochondria, carnosic acid significantly reduced
ethanol-induced apoptosis of hepatocytes. This is attributed to the antioxidant
property of carnosic acid. [150]
Carnosic acid prevents the deposition of β amyloid
plaques in the brain. Thus carnosic acid is useful in prevention of Alzheimer’s
disease. [151]
Acute cyanide poisoning
is life threatening and results in hypoxic brain damage, cardiopulmonary
failure and death within minutes. Chronic cyanide poisoning is a potential
bioterrorist agent. Whether acute or chronic, cyanide intoxication can induce neurological
syndrome including dystonia and Parkinsonian symptoms. CT and MRI studies show
lesions in the basal ganglia, including the globus pallidus and putamen. The
mechanisms involved in neuronal damage are inhibition cytochrome C oxidase,
generation of reactive oxygen species, dysfunctional glutamate transport and
ionic pump failure. Antioxidant property of carnosic acid protects the neurons
from the oxidative stress. [152]
Signal transducer and
activator of transcription 3 (STAT 3) is a transcription factor which in humans
is encoded by the STAT 3 gene. STAT 3 plays a key role in many cellular
processes such as cell growth and apoptosis. Carnosic acid inhibits STAT 3 and
induces apoptosis through generation of reactive oxygen species (ROS) in human colon
cancer HCT 116cells. [153]
Administration of acetaminophen too frequently or in
high doses induces hepatotoxicity. The antioxidant property of carnosic acid
protects the liver against acetaminophen-induced hepatotoxicity. [154]
Carnosic acid alleviates chronic alcoholic liver
injury via anti-steatosis, anti-oxidant and anti-apoptosis effects. [155]
The experimental animals fed carnosic acid experienced
significant weight loss, reduced visceral obesity. In addition there was a
significant reduction in serum cholesterol and triglyceride levels. Importantly
carnosic acid had a dramatic effect on the liver by reducing the hepatic
triglyceride. Additionally carnosic acid improved glucose tolerance. [156]
Several studies suggest that
depression, dementia, autism, obesity, diabetes, lupus, heart disease and
cancer are caused by oxidative stress. By countering oxidative stress, carnosic
acid can prevent and cure the conditions. [157]
Another study shows that the
leaf extract of Rosemary (Rosmarinus
officinalis L.) rich in carnosic acid limits weight gain and improves
cholesterol levels and sugar levels in mice fed on high fat diet. [158]
Serum biochemistry and histological
studies show that in the recommended doses carnosic acid is safe to be used as
a pharmacological agent. In the acute toxicity study on mice showed that, the
oral lethal dose (LD 50) of carnosic acid was 7100 mg/kg body weight. The
histopathological changes were observed in the heart, liver and kidney for the
survival of mice treated with a single dose of carnosic acid. For sub-chronic
toxicity study, carnosic acid administered for 30 days produced slight
reductions in the weight gain pattern, which did not reach the significant
level when compared with the control values. The studies suggest that a
short-term oral administration of carnosic acid has a low toxicity profile. [159]
Vicenin
Molecular
formula: C27H30O15
Structural
formula:
[160]
Vicenin is a water soluble flavonoid glucoside. Three
varieties of vicenin viz. vicenin 1, 2 and 3 are now identified and
isolated.
Of the three vicenin 2 has been investigated
extensively. It has antioxidant, anti-inflammatory, hepatoprotective and anticancer
properties.
Ionizing radiations cause damage to fats, proteins and
DNA resulting in disruption of cell signaling pathways. The result is
cell-cycle disruption, mitotic death and apoptosis. Hence there is a need for
radioprotective compounds.
An ideal radioprotective compound should be effective against
short-term and long-term radiation effects, non-toxic, chemically stable to
permit ease of handling and storage and affordable; and voila! Vicenin is one
such compound. The antioxidant activity of vicenin is said to be cytoprotective
against radiation-induced cell injury. Furthermore flavonoids such as vicenin
appear to facilitate repair of radiation-induced injury. [161]
Transforming growth factor β-induced protein (TGFBIp) is an
extracellular matrix protein. It functions as a mediator of experimental
sepsis. In an experimental study, vicenin-2 reduced cecal ligation and puncture
(CLP)-induced septic mortality and pulmonary injury. Vicenin-2 could be a
potential therapeutic agent for treatment of various severe vascular
inflammatory diseases via inhibition
of transforming growth factor β-induced protein (TGFBIp) signaling pathway. [162]
To evaluate the protective effect of vicenin on bone
marrow, adult Swiss mice were exposed to 0-6 Gy 60Co γ rays 30 min
after an intrapritoneal injection of 50μg/kg body weight of vicenin. The study
showed that vicenin provided efficient protection to the bone marrow against
radiation injury. Thus vicenin provides efficient protection to normal tissues
during radiotherapy for various cancers. [163]
Vicenin-2 has anti-inflammatory effect effect on blood
vessels. Vicenin-2 prevents vasculitis induced by diabetes. Vicenin-2 is also
useful for the treatment of atherosclerosis and other complications of diabetes. [164]
Vicenin-2 is a potent inhibitor of α-glucosidase
inhibitor. Vicenin-2 effectively inhibits the formation of advanced glycation
end products. Vicenin-2 suppresses glycation-induced protein oxidation and the
formation of amyloid plaques. Thus vicenin-2 is useful for the treatment of
diabetes and its complications. [165]
Vicenin-2 effectively inhibited the growth of prostate
tumors in vivo. Vicenin-2 (VCN-2) can be used as a single agent or in
combination with docetaxel (DTL). [166]
A toxicological study on mice
showed that at the dose of 4837.5 mg/kg body weight vicenin-2 had no adverse
effect on the animals.[167]
Sabinene
Molecular formula: C10H16
Structural formula:
[167]
Sabinene is an aromatic,
bicyclic monoterpene. Apart from Tulsi (Ocimum
tenuiflorum) sabinene can be found in pine plnts, black current, black
pepper, nutmeg and many spice plants, oranges etc. Sabinene shows anti-inflammatory,
antioxidant, free radical scavenger and antibacterial activities.[168]
Sabinene found in essential
oil of Tulsi- Basil (Ocimum tenuriflorum)
showed a potent nitric oxide (NO)-scavenging effect and antifungal activity.
The oil was particularly active against dermatophytes and Cryptococcus neopharmans with MIC values ranging from 0.08 to
0.16μL/mL [169]
Sabinene was found to be
toxic to fetus and pregnant hamsters otherwise it showed no toxicity [170]
References
81. Dhanwantari Nighantu, Karawwraadi gana,
50
82.
Kaiyadeva Nighantu, Oushadhi warga, 1554
to 1556
83.
Bhaawapraakash Nighantu, Pushpawarga, 51
84.
Raajanighantu, Karaweeraadiwarga, 150,
151
85. Dr. Kavyashree MR et al, A review on Tulsi (Ocimum sanctum Linn.), Journal of Drug Delivery & Therapeutics,
2019; 9(2-s):562-569
86 https://en.wikipedia.org/wiki/Eugenol
87. Joice Nascimento Bartoza et al, An
overview on the Anti-inflammatory potential and Antioxidant profile of Eugenol,
Oxidative Medicine and Cellular Longevity, Volume 2018, Article ID 3947262
88. https://en.wikipedia.org/wiki/Eugenol
89. Joice Nascimento Bartoza et al, An
overview on the Anti-inflammatory potential and Antioxidant profile of Eugenol,
Oxidative Medicine and Cellular Longevity, Volume 2018, Article ID 3947262
89. Joice Nascimento Bartoza et al, An
overview on the Anti-inflammatory potential and Antioxidant profile of Eugenol,
Oxidative Medicine and Cellular Longevity, Volume 2018, Article ID 3947262
90. https://pubchem.ncbi.nlm.nih.gov/compound/Rosamarinic-acid
91. Rosamarinic Acid- an overview/Science
Direct Topics
https://www.sciencedirect.com>topics>medicine-and-dentistry
92. Tomoki Hase et al, Rosemarinic acid
suppresses Alzheimer’s disease development by reducing amyloid β aggregation by
increasing monoamine secretion, Scientific Reports, 18 June 2019
93. https://journal.restorativemedicine.org, April 1, 2014
94. https://en.wikipedia.org/wiki/Apigenin
95. Minqian Wang et al, A Review on
Apigenin: Dietary Intake, ADME, Antimicrobial Effects and Interactions with
Human Gut Microbiota, BioMed Research International, Volume 2019, Article ID
7010467
96. http://foodb.ca/compounds/FDB013910
98. Sasiporn Sarawek et al,
Pharmacokinetics of Luteolin and Metabolites in Rats, Natural product
Communications, Volume 3(12) 2008
99. Chiu-Yuan Chen et
al, Luteolin suppresses inflammation-associated gene expression by blocking
NF-κB and AP-1 activation pathway in mouse alveolar macrophages, Life Sciences,
Volume 81, Issues 23-24, 30 November 2007, pages 1602-1614
100. D.
Kempuraj et al, Luteolin inhibits myelin basic protein-induced human mast cell
activation and mast cell-dependent stimulation of Jurkat T cells, British
Journal of Pharmacology, Volume 155, Issue 7, December 2008, Pages 1076-1084
101. Gunter
Seelinger et al, Anti-oxidant, Anti-inflammatory and Anti-allergic Activities
of Luteolin, Planta Med 2008; 74(14): 1667-1677
102. Masahiro Kimata et al, Effects of
Luteolin and Other Flavonoids on IgE-Mediated Allergic Reactions, Planta Med
2000; 66(1): 25-29
103. CHEN Min-zhu et al, Effects of
luteolin on inflammation and immune function, Chinese Journal of Pharmacology
and Toxicology, 1986-01
104. D
Papaliodis, The flavonoid luteolin inhibits niacin-induced flush, British
Journal of pharmacology (2008) 153, 1382-1387
105. A.
Miniati et al, Stimulated human melanocytes express and release interleukin-8,
which is inhibited by luteolin: relevance to early vitiligo, Clinical and
experimental Dermatology, 20 June 2013
106. Gloria
Gutierrez et al, Luteolin inhibits lipopolysaccharide actions on human gingival
fibroblasts, European Journal of Pharmacology, Volume 541, Issues 1-2, 10 July
2006, Pages 95-105
107. An-Chin
Cheng et al, Induction of apoptosis by luteolin through cleavage of Bcl-2
family in HL-60 cells, European Journal of Pharmacology, Volume 509, Issue 1,
10 February 2005, Pages 1-10
108. Crasci
L et al, Antidegenerative effect of Apigenin, Luteolin and Quercetin on human
keratinocyte and chondrocyte cultures: SAR evaluation, Drug Res (Stuttg) 2018
Mar; 68(3): 132-138
109. Bartolomeo
Bertolino et al, Beneficial Effects of Co-Ultramicronized
Palmitoylethanolamide/Luteolin in a Mouse Model of Autism and in a Case 110. Report
of Autism, CNS Neuroscience and Therapeutics, Volume 23, Issue 1 January 2017
Pages 87-98
111. BeiXu
et al, Luteolin promotes long-term potentiation and improves cognitive function
in chronic cerebral hypoperfused rats., European Journal of Pharmacology,
Volume 627, Issues 1-3, 10 February 2010, Pages 99-105
112.
Mei-Lin Shen et al, Luteolin inhibits GABAA receptors in HEK cells
and brain slices, Scientific Reports Volume 6, Article number: 27695 (2016)
113. Rufi Tambe et al, Assessment of
luteolin isolated from Eclipta alba leaves in animal models of epilepsy,
Journal Pharmaceutical Biology, Volume 55, 2017, Issue 1
114. KojiHara et al, Effects of intrathecal
and intracerebroventricular administration of luteolin in rat neuropathic pain
model, Pharmacology Biochemistry and Behavior, Volume 125, October 2014, Pages
78-84
115. A Young Choi et al, Luteolin induces
apoptosis through endoplasmic reticulum stress and mitochondrial dysfunction in
Neuro-2a mouse neuroblastoma cells, European Journal of Pharmacology, Volume
668, 1-2, 1 October 2011, Pages 115-126
116. Henry wing-Cheung Leung, luteolin
induced DNA damage leading to human squamous carcinoma CH27 cell apoptosis,
European Journal of Pharmacology, Volume 508, Issues 1-3, 31 January 2005,
Pages 77-83
117. Poyil Pratheeshkumar et al, Luteolin
inhibits Cr(VI)-induced malignant cell transformation of human lung epithelial
cells by targeting ROS mediated multiple cell signaling pathways, Toxicology
and Applied Pharmacology Volume 281, Issue 2, 1 December 2014, Pages 230-241
118. Zhuan Hong Xiang Cao, Luteolin is
effective in the non- small cell lung cancer model with L858R/T790MEGF receptor
mutation and erlotinib resistence, British Journal of Pharmacology Volume 71,
Issue 11 June 2014 Pages 2842-2853
119. Yuanyuan Luo et al, Luteolin: A
flavonoid that has multiple cardio-protective effects and its molecular
mechanisms, Front. Pharmacol. 06 October 2017
120. Fang F et al, Luteolin inhibits
apoptosis and improves cardiomyocyte function through the PI3K/Akt pathway in
simulated ischemia-reperfusion, Pharmacology 2011; 88:149-158
121. Yasong Lang et al, Luteolin inhibited
hydrogen peroxide-induced vascular smooth muscle cells proliferation and
migration by suppressing the Src and Akt signaling pathways, Journal of
Pharmacy and Pharmacology, Volume 64, Issue 4 April 2012 Pages 579-603
122. Jin-HoKim et al, Luteolin prevents
PDGF-BB-induced proliferation of vascular smooth muscle cells by inhibition of
PDGF β-receptor phosphorylation, Biochemical Pharmacology Volume 69, Issue 12,
15 June 2005, Pages 1715-1721
123. Ling-BoQian, Luteolin reduces high
glucose-mediated impairment of endothelium-dependent relaxation in rat aorta by
reducing oxidative stress, Pharmacological Research, Volume 61, issue 4, April
2010, Pages 287-287
124. Jiang Hui-di et al, Vasodilation
effect of luteolin on rat thoracic aorta and its mechanism, Chinese
Pharmaceutical Journal, 2005-06
125. LinglingQi et al, Luteolin improves
contractile function and attenuates apoptosis following ischemia-reperfusion in
adult rat cardiomyocytes, European Journal of Pharmacology, Volume 668, Issues
1-2, October 2011, Pages 201-207
126. Wang Liyan, Pharmacological Study of
Semi-Synthetic Luteolin in Reducing blood pressure, Chinese Pharmacology
Bulletin 1986-02
127. Minghui Tai et al, Protective effect
of luteolin against acetaminophen-induced acute liver failure in mouse,
International Immunopharmacology, Volume 27, Issue 1, July 2015, Pages 164-170
128. Herng-JiunLee et al, Induction
apoptosis of luteolin in human hepatoma HepG2 cells involving mitochondria
translocation of Bax/Bak and activation of JNK, Toxicology and Applied
Pharmacology, Volume 203, Issue 2, 1 March 2005 Pages 124-131
129. Natthawan Kittiratphatthana et al,
Luteolin induces cholangiocarcinoma cell apoptosis through the
mitochondrial-dependent pathway mediated by reactive oxygen spaeies, Journal of
Pharmacy and Pharmacology, Volume 68, Issue 9, September 2016, Pages 1184-1192
130. Luigi Quintieri et al, Flavonoids
diosmetin and luteolin inhibit midazolam metabolism by human liver microsomes
and recombinant CYP3A4 and CYP3A5 enzymes, Biochemical Pharmacology, Volume 75,
Issue 6, 15 March 2008, Pages 1426-1437
131. Guoguang Wang et al, Luteolin
ameliorates cardiac failure in type I diabetic cardiomyopathy, Journal of
Diabetes and its Complications, Volume 26, Issue 4 July-August 2012, Pages
259-265
132. Hany M. et al, Chrysin and Luteolin Attenuate
Diabetes-Induced Impairment in Endothelial-Dependent Relaxation: Effect on
Lipid Profile, AGEs, and NO Generation, Phytotherapy Research, Volume 27, Issue
11 November 2013, Pages 1678-1684
133. Y-T Huang et al, Effects of luteolin
and querctin, inhibitors of tyrosine kinase, on cell growth and
metastasis-associated properties in A431 cells overexpressing epidermal growth
factor receptor, BJP, 1999 Nov, 128(5) 999-1010
134. Yong Lin et al, Luteolin, a flavonoid
with potentials for cancer prevention and therapy, Current Cancer Drug Targets,
2008 Nov 8(7) 634-646
135. https://en.wikipedia.org/wiki/Beta-Sitosterol
136. Jannett Nguyen MD et al, Hair
Supplements, Alopecia, 2019, Botanical Products
137. David Rakel,
https://www.webmed.com/vitamins/ai/ingredientmono-939/beta-sitosterol
141. Daniel Poeckel et al, Carnosic acid
and carnosol potently inhibit human 5-lipooxygenase and suppress
pro-inflammatory responses of stimulated human polymorphonuclear leukocytes,
Biochemical Pharmacology, Volume 76, Issue 1, 1 July 2008, Pages 91-97
142. Julia Baur et al, Carnosol and
Carnosic Acids from Salvia officinalis Inhibit Microsomal Prostaglandin E2
Synthase-1, Journal of Pharmacology and Experimental Therapeutics, July
2012, 342 (1) 169-176
143. Jueun Oh et al, Syk/Src
Pathway-Targeted Inhibition of Skin Inflammatory Responses by Carnosic Acid,
Mediators of Inflammation Volume 2012, Article ID 781375
144. Yuan Ganjun et al, Anti-MRSA Activity
of Carnosic Acid in Rosemary, Chinese-Journal of Modern Applied Pharmacy
2012-07
145. Shanmugam Manoharan, Carnosic acid: A
potent chemopreventive agent against oral carcinogenesis, Chemico-Biological
Interactions Volume 188, Issue 3, 5 December 2010, Pages 616-622
146. Margot
Loussouarn et al, Carnosic acid and Carnosol, Two Major Antioxidants of
Rosemary act through Different Mechanisms, Plant Physiology, November 2017
147. Shanmugam Manoharan S,
Anti-clastogenic potential potential of carnosic acid against 7,12-dimethylbenz(a)nthracene
(DMBA)-induced clastogenesis, Pharmacological Reports Volume 62, Issue 6,
Nov-Dec 2010, 1170-1177
148. Yoko Yagishita et al, NRF2-Mediated
Gene Regulation and Glucose Homeostasis, Molecular Nutrition and Diabetes, 2016
149. Sonjit Das et al, Carnosic acid, a
Natural Diterpene, Attenuates Arsenic-Induced Hepatotoxicity via Reducing
Oxicity Stress, MAPK Activation and Apoptotic Cell Death Pathway, Oxidative
Medicine and Cellular Longevity, Volume 2018/Article ID 1421438
150. Xinyao Tian, Carnosic acid attenuates
acute ethanol-induced liver injury via a SIRT1/p66Shc-mediated mitochondrial
pathway, Canadian Journal of Physiology and Pharmacology, 2016, 94(4): 416-425
151. H. Rasoolijazi et al, The Protective
Role of Carnosic Acid against Beta-Amyloid Toxicity in Rats, The Scientific
World Journal, Volume 2013, 917082
152. Lipton
et al, Protection of Brain Injury from Cyanide Poisoning by Carnosic Acid,
Stanford-Burnham Medical Research Institute, La Jolla, CA, U.S.
153. Do-Hee-Kim,
Carnosic acid inhibits STAT 3 signalling and induces apoptosis through
generation of ROS in human colon cancer HCT 116 cells, Molecular
carcinogenesis, 08 July 2015
154. Qi Guo et al, Carnosic acid protects
against acetaminophen-induced hepatotoxicity by potentiating Nrf2-mediated
antioxidant capacity in mice, Korean J Physiol Pharmacol, 2016 Jan; 20(1):
15-23
155. Lili Gao et al, Carnosic acid
alleviates chronic alcoholic liver injury by regulating the SIRT1/ChREBP and
SIRT1/p66shc pathway in rats, Molecular Nutrition, 29 April 2016
156. Ting Wang, Carnosic acid prevents
obesity and hepatic steatosis in ob/ob
mice, Hepatology Research, 30 December 2010
157. Mohsen Hamidpour,
Chemistry, Pharmacology and Medicinal Property of Sage (Salvia) to Prevent and Cure Illnesses such as Obesity, Diabetes,
Depression, Dementia, Lupus, Autism, Heart Disease and Cancer, Journal of
Traditional and Complimentary Medicine, Volume 4, Issue 2, April-June 2014,
Pages 82-88
158. Alvin Ibarra et al, Carnosic acid-rich
rosemary (Rosamarinus officinalis L.)
leaf extract limits weight gain and improves cholesterol levels and glycaemia
in mice on a high-fat diet, British Journal of Nutrition Volume 106, Issue 8,
28 October 2011, pp 1182-1189
159. Wang QL et al, Acute and 30-day oral
toxicity studies of administered carnosic acid, Food Chem Toxicol. 2012 Dec;
50(12): 4348-4355
160. https://pubchem.ncbi.nlm.nih.gov/compound/Vicenin
161. Satyamitra et al, The antioxidant Flavonoids, Orientin and Vicenin
Enhance Repair of Radiation-induced Damage, SAJ Pharma Pharmacol 1: 105, 20
August 2014
162. Wonhwa Lee, Ameliorative Effect of
Vicenin-2 and Scolymoside on TGFBIp-Induced Septic Responses, Inflammation
Volume 38, Pages 2166-2177 (2015)
163. Nayak V. and Uma Devi P. Protection of
Mouce Bone Marrow against Radiation-Induced Chromosome Damage and Stem Cell
Death by Ocimum Flavonoids Orientin Vicenin, Radiat. Res. 163, 165-171 (2005)
164. Sae-Kwang Ku, Vicenin-2 and
scolymoside inhibit high-glucose-induced vascular inflammation in vitro and in
vivo, Canadian Journal of Physiology and pharmacology, 2016; 94(3): 287-295
165. Hyun AhJung, Vicenin 2 isolated from
Artemisia capillaries exhibited potent anti-glycation properties, Food and
Chemical Toxicology, Volume 69, July 2014, Pages 55-62
166. Lokesh
Dalasanur Nagaprashantha et al, Anti-cancer Effectss of Novel Flavonoid
Vicenin-2 as a Single Agent and in Synergistic Combination with Docetaxel in
Prostate Cancer, Biochemical Pharmacology, 2011 Nov 1, 82 (9) 1100-1109
167. Amit
D. Kandhare, Acute and repeated doses (28 days) oral toxicity study of
Vicenin-1, a flavonoid glycoside isolated from fenugreek seeds in laboratory
mice, Regulatory Toxicology and Pharmacology Volume 81, November 2016, Pages
522-531
168. https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/sabinene,
169. Valente J et al,
Antifungal, antioxidant and anti-inflammatory activities of Oenanthe crocata L.
essential oil, Food Chem Toxicol 2013 Dec; 62:349-354
170.Robert Tisserand
and Rodney Young PhD, Essential Oil Safety (Second Edition) 2014
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