Phtopharmacology of Tulsi-Basil (Ocimum sanctum) Part 4
Phtopharmacology of Tulsi-Basil (Ocimum sanctum) Part 4
Properties and Pharmacology
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,
Kaphahara: Reduced expectoration
Durgandhihara: Relieves various types of foul smells 
Krumidoshahara: Anthelmintic 
Daahawardhinee: Increases burning sensation
Agniwardhinee: Improves appetite and digestion
Shwaasahara: Relieves breathlessness, Bronchitis, Bronchial asthma
Hidhma (Hikkaa) Shaamaaka: Relieves hiccup (Hiccough)
Vami (Chhardi) jit/ Vamihara : Relieves vomiting
Mootrakricchra: Burning micturition
Ashmaree: Urinary stones
Netraroga: Ophthalmic disorders
Vishghna: Antitoxic 
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)
Krucchrajit: Useful for burning micturition 
Shanti krut: Imparts (mental) peace
Druk-krut: Beneficial for vision
Bhootahara: Useful in psychiatric illnesses 
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 
Molecular formula: C10H12O
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. 
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. 
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. 
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. 
Molecular formula: C18H16O8
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. 
Rosamarinic acid (RA) suppresses amyloid β (A β) accumulation in mice thus preventing the development of Alzheimer’s disease. 
Rosamarinic acid reduces inflammations and various allergic conditions
Rosamarinic acid is a novel agent useful in the treatment of autoimmune diseases 
Molecular formula: C15H10O5
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. 
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. 
Molecular formula: C10H14O
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. 
Molecular formula: C15 H 10 O6
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
Anti-degenerative activity of Luteolin
By virtue of its antioxidant, anti-glycative and anti-degenerative properties, luteolin exhibits antiaging property. 
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 , 
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. 
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. 
By reducing oxidative stress luteolin was found to be effective in the treatment of epilepsy. 
Luteolin relieves neuropathic pain via GABAA receptor and opioid receptor 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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. 
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 
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. 
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. 
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. 
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. 
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. 
Molecular formula: C29H50O
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. 
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. 
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.
Systemic lupus erythematosus (SLE)
Chronic fatigue syndrome
Respiratory disorders: β-sitosterol is useful for the treatment of bronchitis, cough of unknown etiology, tuberculosis and bronchial asthma
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.
Other conditions 
Molecular formula: C20H28O4
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. 
In experimental study, anti-inflammatory property of carnosic acid was found to protect white blood cells from developing leukemia. 
By inhibiting microsomal prostaglandin E2 Synthase-1, carnosic acid exhibits a potent anti-inflammatory activity. 
Another study showed that anti-inflammatory property of carnosic acid is useful for treating inflammatory and infective skin diseases and various types of arthritis. 
Carnosic acid shows anti-methicillin resistant staphylococcus aaureus (anti-MRSA) activity. Carnosic acid shows synergistic or additive effect with ampicillin and oxacillin. 
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. 
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. 
7,12-dimethylbenz[a]nthracece (DMBA) exerts destructive effect on bone formation (clastrogenesis). Anti-oxidant property of carnosic acid exerts anti-clastogenic effect. 
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. 
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. 
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. 
Carnosic acid prevents the deposition of β amyloid plaques in the brain. Thus carnosic acid is useful in prevention of Alzheimer’s disease. 
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. 
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. 
Administration of acetaminophen too frequently or in high doses induces hepatotoxicity. The antioxidant property of carnosic acid protects the liver against acetaminophen-induced hepatotoxicity. 
Carnosic acid alleviates chronic alcoholic liver injury via anti-steatosis, anti-oxidant and anti-apoptosis effects. 
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. 
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. 
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. 
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. 
Molecular formula: C27H30O15
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. 
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. 
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. 
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. 
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. 
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). 
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.
Molecular formula: C10H16
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.
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 
Sabinene was found to be toxic to fetus and pregnant hamsters otherwise it showed no toxicity 
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