HOMOEOPATHIC USES OF CURCUMA LONGA

Botanical name    -                       Curcuma longa Linn

Family          -                                   Zingiberaceae

Common names-                          Eng- Turmeric, Hindi-Haldi, Mal- Manjal, Tamil- Manjal

Description-                                              A perennial herb with cylindrical or oblong root tubers , dull yellow flowers

Distribution-                                             Distributed in Thailand, Malay Archipelago and North Australia. In India it is cultivated in Andhra Pradesh, Bihar, Kerala , Maharashtra, Orissa, and Tamil nadu

Part used-                                       Rhizomes

Pharmacology:

Constituents: Curcumin (diferuloylmethane), a polyphenol compound responsible for the bright yellow color of turmeric, is believed to be the principal pharmacological agent. It is prepared from the roots of Curcuma longa. In addition to curcumin, turmeric contains the curcuminoids atlantone, bisdemethoxycurcumin, demethoxycurcumin, diaryl heptanoids, and tumerone. Turmeric also contains sesquiterpenoids⁷ and the constituent ar-tumerone. Other constituents include sugars, resins, proteins, vitamins, and minerals (including iron and potassium).

Alzheimer's effects: Beta-Amyloid (betaA)-induced oxidative stress is a well-established pathway of neuronal cell death in Alzheimer's disease.² Three curcuminoids from turmeric (Curcuma longa L.), including curcumin, demethoxycurcumin, and bisdemethoxycurcumin, were found to protect PC12 rat pheochromocytoma and normal human umbilical vein endothelial (HUVEC) cells from betaA(1-42) insult. These compounds may protect the cells from betaA(1-42) insult through antioxidant pathways. Other animal studies of Alzheimer's disease also suggest that curcumin may reduce levels of amyloid and oxidized proteins and prevent cognitive deficits.¹ One alternative mechanism of action for these effects suggested by Baum et al. is metal chelation, which may reduce amyloid aggregation or oxidative neurotoxicity. Since curcumin more readily binds the redox-active metals and than the redox-inactive , curcumin might exert a net protective effect against beta toxicity or might suppress inflammatory damage by preventing metal induction of NF-kappaB. Mouse studies that evaluated the effects of dietary curcumin on inflammation, oxidative damage, and plaque pathology demonstrated that both low and high doses of curcumin significantly lowered oxidized proteins and interleukin-1beta, which is a proinflammatory cytokine elevated in the brains of these mice. Low-dose but not high-dose curcumin treatment has been shown to reduce the astrocytic marker GFAP and significantly decrease insoluble beta-amyloid (Abeta), soluble Abeta, and plaque burden by 43-50%. However, levels of amyloid precursor (APP) in the membrane fraction were not reduced.

Antibacterial effects: The ethyl acetate extract of Curcuma longa L. has demonstrated a higher antibacterial activity than the methanol extract or water extract.

Anti-inflammatory effects: Turmeric has been associated with the inhibition of tumor necrosis factor-α, interleukin-8, monocyte inflammatory protein-1, interleukin-1B, and monocyte chemotactic protein-1 Turmeric and its constituent curcumin have been found to inhibit lipoxygenase and cyclooxygenase in rat tissues and in vitro, as well as thromboxane B₂¹⁹ and leukotriene B4 formation Based on animal study, oral administration of curcumin may reduce expression of several cytokines, chemokines, and proteinases known to mediate aneurismal degeneration. In rat macrophages, curcumin inhibits the incorporation of arachidonic acid into membrane lipids, as well as prostaglandin E2, leukotriene B4, and leukotriene C4, but does not affect the release of arachidonic acid  Curcumin also inhibits the secretion of collagenase, elastase, and hyaluronidase. Inhibition of neutrophil function has been noted, and in vitro research demonstrates that curcumin inhibits 5-hydroxy-eicosatetraenoic acid (5-HETE) in intact human neutrophils. Turmeric has been found to block cytokine-induced transcription of leukocyte adhesion molecules ICAM-1, VCAM-1, and E-selectin, and it appears to induce the production of endogenous TGF-B1 in animal wounds. Curcumin down-regulates transcription of genes responsible for the production of chemotactic cytokines in bone marrow stromal cells Curcumin reduces chemically-induced rat paw edema and liver inflammation

 Antioxidant effects: Turmeric has been reported to possess antioxidant properties in vitro and in animal studies. Turmeric preparations have been found to scavenge free radicals (peroxides) and phenolic oxidants, inhibit lipid peroxidation induced by chemical agents and inhibit iron-dependent lipid peroxidation in rat tissues. In vitro research shows that turmeric may prevent oxidative damage to DNA and may be a potent scavenger of nitric acid. Curcumin appears to generate a hydroxyl radical. Structural features of curcuminoids that may contribute to antioxidant activity include phenolic and methoxy groups on phenyl rings and diketones. Research using aqueous extracts of turmeric suggests that curcumin is not the only antioxidant in turmeric , and turmerin has been identified as a water-soluble peptide from turmeric with antioxidant properties . Animal studies have reported the reversal of hepatonecrosis and fatty changes associated with turmeric, with reversal of aflatoxin-induced liver damage.

Anti-platelet aggregation effects: Curcumin inhibits thromboxane A2 without affecting the synthesis of prostaglandin I2 In vitro, curcumin inhibits platelet aggregation induced by ADP, epinephrine, or collagen. Turmeric appears to inhibit arachidonic acid incorporation into platelet phospholipids, degradation of phospholipids, and cyclooxygenase. 

 Anti-proliferative effects: Multiple pre-clinical studies have explored potential anti-cancer mechanisms of curcumin

Lipid-lowering effects: In rat models of hyperlipidemia, a diet of 0.5% curcumin for eight weeks significantly lowered serum low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), total cholesterol, and triglyceride levels, possibly by enhancing the activity of hepatic cholesterol-7a-hydroxylase and increasing cholesterol catabolism. The turmeric constituents demethoxycurcumin, bisdemethoxycurcumin, and acetylcurcumin appear to inhibit -stimulated lipid peroxidation in rat tissues and liver microsomes In a rat model of hyperlipidemia, a 50% ethanolic extract of turmeric was associated with a significant reduction in the ratio of total cholesterol to phospholipids. In rabbits fed a high cholesterol diet, oral turmeric (1.6-3.2mg/kg) was associated with lower levels of plasma cholesterol and triglycerides than a control group, although no differences in atherogenesis were noted on histological examination of aortas. Cholesterol levels were lower in the 1.6mg/kg group

Gastro-protective effects: Oral administration of turmeric to rats (500mg/kg) significantly reduces the incidence of chemically-induced duodenal ulcers and is associated with an increase in intestinal wall mucus and non-protein sulfhydryl content. However, early research in guinea pigs reported that various constituents of turmeric do not protect against histamine-induced gastric ulcerations.

Gallbladder effects: Gallbladder contraction over the two-hour period following the administration of 20mg curcumin has been demonstrated in humans. Animal research reports that curcumin in the diet reduces the incidence of chemically-induced gallstones in mice.

Hypoglycemic effects: Based on animal study, both curcuminoids and sesquiterpenoids in turmeric may exhibit hypoglycemic effects via PPAR-gamma activation

Weight loss effects: In a rat study that investigated a Chinese herbal formulation called Number Ten for weight loss, leptin and body fat decreased significantly in the treatment group compared to the control group (p<0.009 and p<0.006, respectively).

Other effects: Chelation: In vitro research on liposomal membranes has demonstrated that curcumin forms chelates with iron. Phototoxicity: Curcumin in low concentrations has been found to potentiate phototoxicity to the bacteria S. typhimurium and E. coli

Homoeopathic use--Cardiovascular complaints, Liver complaints, Increased cholesterol levels, Rheumatism, Backache, Diarrhea, Constipation, Voracious appetite, Gingivitis, Vertigo, Eye inflammation , Lachrymation

GLYCERRHIZA GLABRA PHARMACOLOGY AND HOMOEOPATHIC USES

Botanical name- Glycerrhiza glabra Linn

Family- Leguminoceae

Common name- English- Liquorice, Hindi- Madhuyashti, Sanskrit- Madhuka

Description – It is a native of Southern Europe. A perinneal herb 1-1.5 mtrs in height. Root long, reddish yellow, root and bark give multiple branches. Leaves- compound leaflets. Flowers – pinkish. Pods- 3 cm long, flat. It contains 2-5 squared seeds. Flowers in summer and seeds in rainy season

Part used – Roots

Chemical constituents- Triterpene saponins-Glycyrrhizin (glycyrrhizic acid) is the major saponin, responsible for the sweet taste of liquorice, and its aglycone, glycyrrhetinic acid; together with other derivatives and glycosides such as glycyrrhizol, glabrins A and B, glycyrrhetol, glabrolide, isoglabrolide and others.

Flavonoids and Isoflavonoids - Liquiritin, which during drying and storage undergoes partial conversion to isoliquiritin; their aglycones, liquiritigenin and isoliquiritigenin, isolicoflavonol, licoagrodione, glucoliquiritin apioside, prenyllicoflavone A, shinflavone, shinpterocarpin, I-methoxyphyaseollin and rhamnoliquirilin. A variety of isoflavones are also reported form the plant, including formononetin, glabrene, neoliquiritin, hispaglabridin A and B, glabridin, glabrol, 3-hydroxyglarol, glycyrrhisflavone, 4-0-methylglabridin, 3' -hydroxy-4' -0-methylglabridin and many 2-methyl isoflavones.

Coumarins and coumestan drivatives-Herniarin, umbelliferone, C-liqucoumarin, 6-acetyl-5,hydroxy-4-methyl coumarin, glycycoumarin and licopyanocoumarin have been identified.

Phytosterols -Stigmasterol, onocerin, β-Sitosterol and β-amyrin.

Volatile oils --Liquorice contains a trace amount (0,5%) of volatile oil, containing anethole, estragole, eugenol and hexanoic acid as the main constituents.

Traditional uses-It is used as a tonic, laxative, demulcent, expectorant and emollient in many traditional systems of medicine. It finds particular use in cough, catarrh, bronchitis, fever, gastritis, gastric and duodenal ulcers and skin diseases and as a general tonic. It has been applied externally to cuts and wounds and used in the treatment of hyperdipsia, genitourinary diseases and many other minor indications, including as a corticosteroid replacement agent.

Medicinal and pharmacological action-Antiulcer activity: Liquorice has a well-documented antiulcer action, being as effective as cimetidine and pirenzapine in curing peptic ulcer. An Ayurvedic preparation containing liquorice increased β-glucuronidase activity in the Brunner's glands, offering protection against duodenal ulcer.

Hepatoprotedive activity: Liquorice is used traditionally for the prevention of liver diseases. Administration to experimental animals increased the duration of the lag phase of ascorbate free radical oxidation in the liver and myocardium, the antioxidant activity of the root powder being comparable to that of I)-carotene, and markedly decreased lipid peroxides in liver. An alcoholic extract increased the cumulative biliary and urinary excretion of acetaminophen without affecting the thioether or sulphate conjugates and also increased glucuronidation in rats, suggesting it may intluence detoxification of xenobiotics.

Antioxidant adivity: An investigation using the isotlavonoids of liquorice focused on their ability to protect the liver mitochondria against oxidative stresses. This effect was linked with the inhibition of mitochondrial lipid peroxidation-related respiratory electron transport. Glabridin and its derivatives contributed to the antioxidant activity induced by heavy metal ions and macrophages against low density lipoprotein (LDL) oxidation. LDL oxidation is a major factor in the production aetiology of early arteriosclerosis. The isotlavans also showed a potent scavenging effect on the DPPH radical and were able to chelate heavy metals. This action was associated with the hydroxy functional group as well as the hydrophobic moiety of the isotlavans. Glabridin also inhibited the susceptibility ofLDL to oxidation in an atherosclerotic apolipoprotein E deficient and in vitro human LDL oxidation model and prevented the consumption of I)-carotene and lycopene. Further experiments with glabridin and accompanying isotlavans suggested that glabridin is a potent inhibitor of cholesterollinoleate hydroperoxide formation.

Antimicrobial adivity: Extracts containing tlavonoids showed significant antimycotic activity when evaluated using strains of Candida albicans isolated from clinical samples of acute vaginitis. Flavonoid constituents isolated from liquorice hairy root cultures also exhibited antimicrobial activity when tested by the disc diffusion method. Hispaglabridin A and B, glabridin, glabrol, 3-hydroxyglabrol and 4' -O-methylglabridin have demonstrated significant antimicrobial activity.

Anticancer adivity: Liquorice potentiated the antitumour and antimetastatic activity of cyclophosphamide when tested in . metastasising Lewis lung carcinoma. Extracts have been assayed for cytotoxicity in vitro using the Yoshida ascites sarcoma; the petroleum ether extract exhibited a more potent activity than other solvent extracts. Liquorice has also been shown to protect against skin tumorigenesis caused by DMBA (7,12-dimethyl-benz [a] anthracene) initiation and 12-0-tetradecanoylphorbol-13-acetate (TPA) promotion. The latency period of tumour onset was increased and the number of tumours decreased, possibly by inhibiting the carcinogen metabolism after DNA adduct formation.

Antimutagenic adivity: Glycyrrhiza glabra root and its isolated constituents were tested against ethyl methanesulphonate, N-methyl-N' -nitro- N -nitrosoguanidine and ribose-lysine Maillard models of mutagenesis using a Salmonella microsome reversion assay. The extract showed antimutagenic activity against ethyl methanesulphonate and 18-β glycyrrhetinic acid exhibited a significant des mutagenic activity against ribose-lysine mutagenic browning mixture.

Antiinflammatory adivity: Glycyrrhizin inhibited thrombin-induced platelet aggregation, which indicates antiinflammatory activity. It also prolonged plasma recalcification and fibrogen clotting times. Glyderinine, a derivative of glycyrrhizic acid, reduced inflammation via the adrenal cortex, suppressed vascular permeability and allergic and antipyretic activity, without causing haemopoiesis or ulceration.

HOMOEOPATHIC USES –

·         Used as anti-inflammatory and expectorant

·         Useful in irritating cough, sore throat, cold and bronchitis

·         Research found it useful like corticosteroids without their side effects

·         Inhibits the growth of prostate cancer 

·         Helps in reduction of body fat- reduces blood cholesterol

·         Used for oligospermia, increases sperm count