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| Year : 2008 | Volume
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| Issue : 3 | Page : 164-169 |
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| Anti-hepatotoxic and anti-oxidant defense potential of Tridax procumbens |
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Reddipalli Hemalatha
Department of Pharmaceutical Technology, Noida Institute of Engineering and Technology, 19, Institutional Area, Knowledge Park-II, Greater Noida, Gauttambudh Nagar, UP - 201 307, India
Click here for correspondence address and email
| Date of Submission | 03-Apr-2008 |
| Date of Acceptance | 23-Jun-2008 |
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 Abstract | | |
Tridax procumbens is a widely occurring medicinal herb used by ethnomedical practitioners. With increased use of chemicals and alcohol besides growing incidence of viruses and autoimmune diseases, the incidence of liver injury is growing for which conventional drugs used for treatment are often inadequate. Various models are adopted in pharmological studies for inducing hepatitis/ liver injury similar to those observed in human viral hepatitis, diabetes and oxidative stress. D-galactosamine with lipopolysacchride (LPS), carbontetrachloride (CCl 4 ) and paracetamol intoxication, diabetes induced with alloxan are widely used on rodents for this purpose.
In vitro studies on Tridax procumbens (TP) revealed the anti-oxidant potential of the herb with chloroform fraction of the ethanolic extract showing maximum activity. It is also reported to possess anti-oxidant minerals such as iron, magnesium, copper and zinc. In vivo studies on rodents on the anti-oxidant potential of TP induced through LPS, CCl 4, alloxan and paracetamol intoxication induced hepatitis confirmed the results from in vitro studies as a potential anti-hepatotoxic herb. Keywords: Anti-hepatotoxicity, anti-oxidant, ethanolic extract, Tridax procumbens
How to cite this article:
Hemalatha R. Anti-hepatotoxic and anti-oxidant defense potential of Tridax procumbens. Int J Green Pharm 2008;2:164-9 |
| Introduction | |  |
The largest organ in the human body, liver, plays a very important role in the metabolism of foreign compounds entering the body. The exposure to the foreign compounds may be through consumption of alien/ contaminated foods, from exposure to chemical substances in the occupational environment or through synthetic drugs consumed for various pathological conditions. These compounds have many toxic manifestations on the human liver. [1] In humans, hepatitis or liver injury is also caused by viruses, chemicals, alcohol and autoimmune diseases. Liver diseases remain one of the serious health problems and medicinal plants and herbs have been in use for treating these, in the Indian traditional systems of medicine especially Ayurveda. The present modern age demands proof on a scientific basis to justify the various medicinal uses of herbs. [2] Although the biologically active compounds in most of the herbal drugs are unknown, they are being used / prescribed widely because of their effectiveness (ascertained through traditional knowledge) at a relatively low cost and fewer side effects. However, safe drugs for serious liver disorders continues to be an area of interest. [3]
Morbidity and mortality resulting from chronic liver diseases such as hepatitis is a major public health problem worldwide especially in developing countries. The major abnormalities associated with hepatitis are lipidemia, peroxidation and loss of plasma membrane integrity. Search for new drugs for limiting hepatic injury has been of interest recently with the better understanding of the processes involved in hepatitis fuelled by the urgent need for the clinical development of safe and non-toxic cytoprotective agents. [4]
Conventional drugs used in the treatment of liver diseases are often inadequate. It is therefore necessary to search for alternative drugs for the treatment of liver diseases to replace the currently used drugs of doubtful efficacy and safety. India is well known for a plethora of medicinal plants. The medicinal use of many plants (as hepatoprotectants) like Andrographis paniculata, Azadirachta indica, Cassia fistula, Elephantopus scaber, Hibiscus rosasinensis, Phyllanthus debilis, Picrorrhiza kurroa, Glycyrrhiza glabra Linn has been reported in the literature. [1],[5],[6]
Tridax procumbens is one such herb available throughout world. It has been widely used medicinal plant for cuts and wounds and diarrohea which is also a herb of economical importance in many countries.
Pharmacological Models for Inducing Hepatitis
LPS induced hepatitis
Lipopolysacchride (LPS), a component of the outer membrane of Gram-negative bacteria, can cause hepatitis in rodents when it is injected in combination with D-galactosamine (GalN). [7] Hepatitis induced by D-galactosamine (GalN) has been reported to show many metabolic and morphologic aberrations in the liver tissue of the experimental animals similar those observed in human viral hepatitis. [8],[9] It induces hepatic necrosis by a multiple step mechanism. It mainly results from a depression of uracil nucleotide-dependent biosynthesis of nucleic acids, glycolipids, glycoproteins and glycogen, accompanied by organelle injury, necrosis of heptocytes, infiltration by inflammatory cells and accumulation of fat. [10],[11] The LPS-induced hepatis is thought to be mediated by tumor necrosis factor (TNF)-α, which is synthesised and released from macrophages in the liver, including Kupffer cells, the resident macrophages in the liver, in response to LPS.[12] Peroxidation of endogenous lipid is a major factor in the cytotoxic action of GalN. A growing body of evidence is emerging which suggests that reactive oxygen-derived free radicals play a crucial role in the pathogenesis of GalN-induced hepatitis. [13]
In humans, hepatitis or liver injury is caused by viruses, chemicals, alchohol and auto immune diseases. TNF-α has been shown to participate in pathogenesis of virus,[14] alchohol [15] and immune induced [16] hepatitis, and LPS-hepatitis has been used frequently as hepatitis model with GalN sensitized rodents.
It has been generally considered that higher levels of hepatic glutathione are favourable to protect against various types of liver injury, since glutathione is the major antioxidnat and as a conjugation substrate of xenobiotics in the liver. However, it has been reported that the depletion of hepatic glutathione led to protection against certain types of hepatitis, including LPS + GalN and TNF-α + GalN induced hepatitis,[17] rather than aggravating liver injury.
Carbon Tetrachloride Induced Hepatitis
Carbon tetrachloride (CCl 4 ) is often used to induce oxidative stress-related hepatitis. The reactive metabolites such as trichloromethyl (CCl 3 ) and trichloromethyl peroxy (CCl 3 OO) radicals emanated from CCl 4 initiate peroxidation of membrane unsaturated fatty acids. This lipid peroxidation of membrane seriously impairs its function and produces liver injury. [1]
Liver damage induced by CCl 4 is commonly used model for the screening of hepatoprotective drugs. [18] The rise in serum levels of aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) has been attributed to the damaged structural integrity of the liver, because they are cytoplasmic in location and released into circulation after cellular damages. [19] The rise in the levels of serum bilirubin is the most sensitive and confirms the intensity of jaundice. [20] The CCl 4 is converted into reactive metabolite, halogenated free radical by hepatic cytochrome P450s, [21],[22] which in turn covalently binds to cell membrane and organelles to elicit lipid peroxidation with subsequent tissue injury. High lipid peroxidation values indicate excessive free radical induced peroxidation. [23],[24]
The antioxidant enzymes Superoxidedismutase (SOD), catalase (CAT) and peroxidases constitute a mutually supportive team of defense against reactive oxygen species (ROS). [25] The decrease in the activity of SOD in the liver and kidney of CCl 4 -treated rats may be due to the increased lipid peroxidation or inactivation of the enzyme by cross-linking with malondialdehyde. This will cause an increased accumulation of superoxide radicals, which could further stimulate lipid peroxidation. Glutathione-s-transferase (GST) binds to lipophilic compounds and acts as an enzyme for glutathione (GSH) conjugation reactions. [6] The decrease in the activity of GST during CCl 4 toxicity may be due to the decreased availability of GSH and suggests a total inhibition of drug metabolism during CCl 4 -intoxication. Depletion of GSH results in enhanced lipid peroxidation, which in turn causes increased GSH consumption. [6]
Hepatotoxins develop hypoxic conditions which can damage the perivenular zone of the hepatic acinus. The highest expression of Cytochrome P450 2E1 (CYP2E1) in the perivenular region produces oxy-radicals that contribute to the injury. Moreover, hepatocytes in the perivenular area contain less antioxidant factors and antioxidant enzymes. [26] Thus, while the lipid peroxidation mediated by oxy radicals is likely to be the highest in the perivenular area, the detoxifying capacity of the hepatocytes here is reduced, therefore, the production may exceed the detoxification in the perivenular area. In short, CCl 4 -induced damage produces alteration in the antioxidant status of the tissues, which is manifested as an abnormal histopathology.
Durg (paracetamol) Induced Hepatitis
Paracetamol induced intracellular stress, accompanied by changes in the structural and functional characteristics of liver cell membranes, which affects DNA integrity, membrane-bound ATPase and inorganic cations homeostasis. Rats intoxicated with paracetamol showed significant impairment in activities of total ATPase, Mg 2+ -ATPase, Ca + -ATPase and Na + /K + -ATPase, with concomitant changes in the levels of tissue protein thiols and inorganic cations, such as Na + , K + and Ca 2+ . [27]
Alloxan Induced Diabetes and Resulting Oxidative Stress
Alloxan produces diabetes mellitus (DM) causing decrease in insulin level, hyperglycemia, elevated total lipids, triglycerides and cholesterol, decreased high-density lipoprotein and hepatic glycogen contents and elevated hepatic glucose-6-phosphatase activity. Concurrent with these changes, an increase in the concentration of malondialdehyde and 4-hydroxynonenal in the liver is also observed. This oxidative stress was related to a decreased glutathione (GSH) content and superoxide dismutase activity in the liver of alloxan-diabetic rats. [28]
Pharmacological Studies on Anti-oxidant Activities of Tridax Procumbens
In vitro studies
The anti-oxidant activity of Tridax procumbens was studied in vitro through 2,2-diphenyl-picrylhydrazyl hydrate (DDPH) assays. The Cholroform fraction of 96% ethanolic extract showed maximum activity followed by the Ethylacetate fraction of ethanolic extract [29] [Table 1]. The Constituents in these fractions were identified as Flavonoids and Alkaloids. The free radical scavenging activity was further confirmed Spectrophotometrically by beta-carotene and DDPH using 70% methanol extract in which the ethylacetate fraction showing highest activity with IC 50 of 37.39 µg/ml. [30]
Further, Tridax procumbens is also known be rich in anti-oxidant minerals such as Iron (Fe), Copper (Cu), Manganese (Mn) and Zinc (Zn) besides other trace minerals such as Magnesium (Mn), potassium (K) and Calcium (Ca) etc. [31] [Table 2].
In vivo studies on animal models
The anti-oxidant and free radical scavenging potential of TP was studied in vivo on animal models by inducing hepatitis. The studies carried out with various extracts were listed in [Table 3].
LPS Induced Hepatitis
D-GalN (300 mg/kg body weight) and LPS (30 µg/kg body weight)-induced hepatic damage was manifested by a significant increase in the activities of marker enzymes AST, ALT, ALP, lactate dehydrogenase and gamma glutamyl transferase (γ-GT) and bilirubin level in serum and lipids both in serum and liver. Pretreatment of rats with a chloroform insoluble fraction from ethanolic extract of arial parts of Tridax procumbens reversed these altered parameters to normal values. The biochemical observations were supplemented by histopathological examination of liver sections. Results of this study revealed that Tridax procumbens could afford a significant protection in the alleviation of d-GalN/LPS-induced hepatocellular injury. [32]
Further, induction of rats with D-GalN/LPS (300 mg/kg body weight/30 g/kg body weight) led to a marked increase in lipid peroxidation as measured by thiobarbituric acid reactive substances (TBARS) in liver. Further, there was a decline in the activities of enzymic antioxidants such as superoxidedismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione s-transferase (GST) and the levels of non-enzymic antioxidants namely reduced glutathione, vitamin C and vitamin E. These biochemical alterations were normalised upon pretreatment with TP extract at a dose of 300 mg/kg body weight orally for 10 days. [33]
Carbon Tetrachloride Induced Hepatitis
The ethanolic extract of T. procumbens was studied for its hepatoprotective action against CCl 4 . Acute and chronic models of hepatic damage were studied recording morphological, metabolic, histological and biochemical parameters. T. procumbens demonstrated antihepatotoxic action justifying its use in liver affection. The action of ethanolic dry extract of T. procumbens was studied by optical microscope examination of liver section. Administration of Tridax .procumbens did not cause any pathological changes and the liver was normal in appearance, similar to the liver cells of normal rat. The drug also protected the liver against acute CCl 4 toxicity. [34]
Hepatoprotective effect of ethanolic extract of arial parts of T. procumbens and its chloroform soluble and insoluble fractions were studied on acute hepatitis induced in rats by single dose of carbon tetrachloride, 15 ml/kg (1:1 of CCl 4 in olive oil) orally. Hepatoprotective activity was monitored by estimating serum transaminases, serum alkaline phosphatases, serum bilirubin and serum albumin. Only the ethanolic extract and chloroform insoluble fraction exhibited hepatoprotective activity. [35]
Durg (Paracetamol) Induced Hepatitis
Tridax procumbens had a salubrious effect on the paracetamol-induced hepatotoxicity in Wister rats. [36]
The oxidative stress in paracetamol induced hepatic damage in rats was determined by estimating the levels of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), activities of antioxidant enzymes, such as superoxide dismutase (SOD), catalse (CAT), glutathione peroxidase (GPX) and glutathione s-transferase (GST), were assessed in rats of induced hepatic damage, and confirmation of generation of oxidative stress was confirmed by comparing levels of these parameters with control group. Generation of oxidative stress was confirmed by enhanced level of TBARS in toxic group. Reduction in GSH content due to toxicity was nullified by subsequent treatment of rats with Tridax procumbens extract. The decrease in levels of antioxidant enzymes in toxic group thus revealed the damaging effects of free radicals generated due to paracetamol (2g/kg body wt) administration. The activities of these enzymes returned to normal in Tridax procumbens extract administered (300 mg/kg body wt) rats indicating the antioxidant efficacy of the Tridax procumbens extract in relieving oxidative stress. [37]
Oxidative Stress in Diabetic Animals
Oxidative stress plays an important role in chronic complications of diabetes. The antioxidant effect of oral administration of Tridax procumbens whole plant 50% methanolic extract on tissue antioxidant and lipid peroxidation in liver of alloxan induced diabetic rats was evaluated. Administration of 250 mg/kg body wt. of the TP extract for 30 days resulted in a significant reduction in fasting blood glucose and an increase in total hemoglobin. It also prevented decrease in body weight gain. The elevated lipid peroxidation in thiobarbituric acid reactive substances (TBARS) was ameliorated by oral administration of TP extract in diabetic rats; while the decreased activities of key antioxidants such as ascorbic acid, glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in diabetic rats were brought back to near normal range. Amelioration of oxidative stress and antioxidant status by TP in diabetics may be attributed to its antihyperglycemic and immunomodulatory property. The antioxidant potential of TP was comparable with glibenclamide, a standard oral hypoglycemic drug. [38]
| Discussion | | |
The widely occurring rice weed Tridax procumbens is used for various problems related to liver such as Jaundice, icterus, hepatitis, cirrhosis, [39] besides Gastritis and heart burn. [40] Various researchers used different models to find the effect of the herb in alleviating oxidative stress on liver. It has been demonstrated that the chloroform insoluble fraction of ethanol extract is most potent in alleviating the oxidative stress/ liver injury caused by factors similar to viral hepatitis, drug intoxication, and lipid peroxidation due to reactive oxidative species.
Further, it has been demonstrated that Tridax Procumbens possibly activates muscarinic cholinergic receptors [41] which also protects the liver via efferent vagus nerve. However, further studies need to be carried out to study the possible pathway.
Ethno-medical practitioners generally use plant juice for treating ailments for liver as they generally would not have required chemicals, which results in non optimal treatment. Further studies need to be carried out to study the dose related effect on hepatotoxicity. Also further studies need to be carried out with regard to intoxication with other models such as iron, alcohol etc to prove its efficacy.
| Acknowledgement | | |
The author sincerely thanks Dr. S.P. Basu, Director, Noida Institute of Engineering and Technology, Greater Noida for suggesting the topic and extending all help in formulating this article.
| References | | |
| 1. | Rajesh MG. Protective activity of glabra Linn on carbon tetrachloride-induced peroxidative damage. Indian J Pharmacol 2004;36:284-7.  |
| 2. | Pohocha N, Grampurohit ND, Antispasmodic activity of the fruits of Helicteres isora Linn Phytother Res 2001;15:49-52. |
| 3. | Mohan GK, Pallavi E, Ravi Kumar B, Ramesh M, Venkatesh S. Activity of carica, leaf extract against carbon tetrachloride-induced hepatotoxicity in rats. DARU 2007;15:162. |
| 4. | Meena B, Anbin Ezhilan R, Rajesh R, Sheik Hussain A, Ganesan B, Anandan R. Antihepatotoxic potential of Sargassum polycystum (Phaeophyceae) on antioxidant defense status in Dgalactosamine- induced hepatitis in rats. Afr J Biochem Res 2008;2:51-5. |
| 5. | Rajesh MG, Latha MS. Hepatoprotection by Elephantopus scaber Linn in CCl4-induced liver injury. Indian J Physiol Pharmacol 2001;45:481-6. |
| 6. | Anandan R, Deepa Rekha R, Devaki T. Protective effect of Picrorrhiza kurroa on mitochondrial glutathione antioxidant system in D-galactosamine- induced hepatitis in rats. Curr Sci 1999;76:1543-5. |
| 7. | Galanos C, Freudenburg MA, Reutter W. Galatosamine-induced sensitazation to the lethal effects of endotoxin. Proc Natl Sci USA 1979;76L:5939-43. |
| 8. | Anandan R, Devi KP, Devaki T, Govindaraju P. Preventive effects Picrorhiza kurroa on D-galatosamine-induced hepatitis in rats. J Clin Biochem Nutr 1998;25:87-95. |
| 9. | Kucera O, Lotkovα H, Kandαr R, Hιzovα R, Muzαkovα V, Cervinkovα Z. The model of D-galactosamine-induced injury of rat hepatocytes in primary culture. Acta Medica (Hradec Kralove) 2006;49:59-65. |
| 10. | Black DD, Tso P, Weidman S, Sabesin SM. Intestinal lipoproteins in the rat with D-(+)-galactosamine hepatitis. J Lipid Res1983;24:977-92. |
| 11. | Laconi E, Sarma DS, Pani P. Rat hepatocyte nodules are resistant to the necrogenic effect of D-galactosamine. Carcinogenesis 1992;13:2459-61. |
| 12. | Bradham CA, Plumple J, Manna MP, Brenner DA, Trautwein C. Mechanism of hepatic toxicity: I, TNG-induced liver injury, Am J Physiol 1998;275:G387-92. |
| 13. | Ohta Y, Matsura T, Kitagawa A, Tokunaga K, Yamada K. Xanthine oxidase-derived reactive oxygen species contribute to the development of D-galactosamine-induced liver injury in rats. Free Radic Res 2007;41:135-44. |
| 14. | Ando K, Hiroishi K, Kaneko T, Moriyama T, Muto Y, Kayagaki N, et al. Perfoli, Fas-Fas ligand, and TNF-α pathways as specific and bystander killing mechanism of hepatic C virus-specific human CTL. J Immunol 1997;158:5283-91. |
| 15. | Yin M, Wheeler MD, Kono H, Bradford B, Gallucci RM, Luster MI, et al . Essential role of tumor necrosis factor α in alcohol induced liver injury in mice. Gastroenterology 1999;117:942-52. |
| 16. | Gantner F, Leist M, Lohse AW, Germann PG, Tiegs G. Concanavalin A-induced T-cells mediated hepatic injury in mice: The role of tumor necrosis factor. Hepatology 1995;21:190-8. |
| 17. | Hentze H, Gantner F, Kolb SA, Wendel A. Depletion of hepatic glutathione prevents death receptor-dependent apoptotic and necrotic liver injury in mice. Am J Pathol 2000;156:2045-56. |
| 18. | Slater TF. Biochemical mechanism of liver injury. London: Academic Press; 1965. |
| 19. | Sallie R, Tredger JM, William R. Drugs and the liver: Part I, Testing liver function. Biopharm Drug Dis 1991;12:251-9. |
| 20. | Drotman RB, Lawhorn GT. Serum enzymes as indicators of chemically induced liver damage. Drug Chem Toxicol 1978;1:163-71. |
| 21. | Packer JE, Slater TF, Wilson RL. Reactions of the carbon tetrachloride related peroxy free radical (CC 130.2) with amino acids: Pulse radiolysis evidence. Life Sci 1978;23:2617-20. |
| 22. | Van de Straat R, de Vries J, Debets AJ, Vermueulein NP. The mechanism of prevention of paracetomaol-induced hepatotoxicity by 3,5-dialkyl substitution: The role of glutathione depletion and oxidative stress. Biochem Pharmacol 1987;36:2065-70. |
| 23. | Brattin WJ, Glenda EA Jr, Recknagel RO. Pathalogical mechanisms in carbon tetrachloride hepatotoxicity. J Free Radical Biol Med 1985;1:27-38. |
| 24. | Prabakaran M, Rangasamy A, Devaki T. Protective effect of indicus against rifampicin and isoniazid-induced hepatotoxicity in rats. Fitoterapia 2000;71:55-9. |
| 25. | Bandhopadhay U, Das D, Banerjee KR. Reactive oxygen species: Oxidative damage and pathogenesis. Curr Sci 1999;77:658-65. |
| 26. | Kera Y, Sippel HW, Penttila KE, Lindros KO. Acinar distribution of glutathione-dependent detoxifying enzymes: Low glutathione peroxidase activity in perivenous hepatocytes. Biochem Pharmacol 1987;36:2003-6. |
| 27. | Raghavendran HB, Sathivel A, Yogeeta RS, Devaki T. Efficacy of sargassum polycystum (phaeophyceae) sulphated polysaccharide against paracetamol-induced dna fragmentation and modulation of membrane-bound phosphatases during toxic hepatitis. Clin Exp Pharmacol Physiol 2007;34:142-7. |
| 28. | El-Missiry MA, El Gindy AM. Amelioration of alloxan induced diabetes mellitus and oxidative stress in rats by oil of eruca sativa seeds. Nutr Metab 2000;44:97-100. |
| 29. | Nia R, Paper DH, Essien EE, Oladimeji OH, Iyadi KC, Franz G. Investigation into in-vitro radical scavenging and in-vivo anti-inflammatory potential of Tridax Procumbens. Niger J Physiol Sci 2003;18:39-43. |
| 30. | Sukarti E, Hartanti L Daya Antiokeisan Tridax Procumbens L. Available from: http://www.upm.wima.ac.id/emi.pdf. |
| 31. | Ahamefule FO, Obua BE, Ibeauwuchi JA, Udeosen NR. The nutritive value of some plants browsed by cattle in Umudike, South Eastern Nigeria. Pak J Nutr 2006;5:404-9. |
| 32. | Ravikumar V, Shivashangari KS, Devaki T. Hepatoprotective activity of Tridax procumbens against d-galactosamine-lipopolysaccharide-induced hepatitis in rats. J Ethnopharmacol 2005;101:55-60. |
| 33. | Ravikumar V, Shivashangari KS, Devaki T. Effect of Tridax procumbens on liver antioxidant defense system during lipopolysaccharide-induced hepatitis in D-galactosamine sensitised rats. Mol Cell Biochem 2005;269:131-6. |
| 34. | Saraf S, Pathank AK, Dixit VK. Hepatoprotective activity of Tridax procumbens, Part I. Fitoterapia 1991;62:307-17. |
| 35. | Saraf S, Dixit VK. Hepatoprotective activity of Tridax procumbens part-II. Fitoterapia 1991;62:534-6. |
| 36. | Kumar SS, Asokan D, Kumar PS, Kalavathy S, Manoharan N. Salubrious effect of Tridax procumbens on paracetamol hepatotoxicity. J Pharma Sci 2001;63:64-6. |
| 37. | Wagh, SS, Shinde GB. Screening of Antioxidant properties of Tridax procumbens Linn. (Asteraceae) in paracetamol induced hepatotoxicity in male albino rats, 76th annual Meeting confined to all India Life science Scientists. Tirupati: SBCI; 2007. p. AP5. |
| 38. | Pareek H, Sharma S, Khajja BS, Jain K, Jain GC. Tridax ameliorates oxidative stress and altered antioxidant status in alloxan induced diabetic rats, Poster Session. Jaipur: International conf. on Free radicals and Natural Products in health; 14-16, 2008. |
| 39. | Adjanohoun EV, Adjakidje MR, Ahyi. Contribution aux ιtudes ethnobotaniques et floristiques en Rιpublique populaire du Bιnin. Agence de coopιration culturelle et technique. Paris: ACCT; 1989. p. 895. |
| 40. | Glover PE, Stewart J, Gwynne Masai MD. Kipsigis notes on East african plants, Part III - Medicinal uses of plants. East Afr Agri Forest J 1966;32:200-7. |
| 41. | Salahdeen HM, Yemitan OK, Alada AR. A Effect of aqueous leaf extract of Tridax procumbens on blood pressure and rate in rats. Afr J Biomed Res 2004;7:27-9. |
Correspondence Address:
Reddipalli Hemalatha
B-119, Pocket II, Kendriya Vihar, Sector 82, Noida
India
  | 3 |
DOI: 10.4103/0973-8258.42736
[Table 1], [Table 2], [Table 3] |
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