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 RESEARCH ARTICLE
Year : 2009  |  Volume : 41  |  Issue : 1  |  Page : 23-27

Hepatoprotective activity of Eugenia jambolana Lam. in carbon tetrachloride treated rats


1 Department of Pharmacology, Bhupal Nobles' Girls College of Pharmacy, Udaipur, Rajasthan, India
2 Laboratory of Animal Cell Biotechnology, Department of Biotechnology, University College of Science, M. L. S. University, Udaipur, Rajasthan, India

Correspondence Address:
S S Sisodia
Department of Pharmacology, Bhupal Nobles' Girls College of Pharmacy, Udaipur, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0253-7613.48888

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Objective: To estimate the hepatoprotective effects of the methanolic seed extract of Eugenia jambolana Lam. (Myrtaceae), in Wistar albino rats treated with carbon tetrachloride (CCl 4 ). Materials and Methods: Liver damage in rats treated with CCl 4 (1ml/kg/Bw, administered subcutaneously, on alternate days for one week) was studied by assessing parameters such as serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP), acid phosphatase (ACP) and bilirubin (total and direct). The effect of co-administration of Eugenia jambolana Lam. (doses 100, 200 and 400 mg/kg p. o.) on the above parameters was investigated. These biochemical observations were supplemented by weight and histological examination of liver sections. Liv.52® was used as positive control. Data were analyzed by one way anova, followed by Scheff's/Dunnett's test. Results: Administration of Eugenia jambolana Lam. (doses 100, 200 and 400 mg/kg p. o.) significantly prevented carbon tetrachloride induced elevation of serum SGOT, SGPT, ALP, ACP and bilirubin (total and direct) level. Histological examination of the liver section revealed hepatic regeneration, after administration of various doses of Eugenia jambolana Lam. The results were comparable to that of Liv.52®. Conclusion: The study suggests preventive action of Eugenia jambolana Lam. in carbon tetrachloride induced liver toxicity. Hepatic cell regeneration process was dose dependent.






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