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 RESEARCH PAPER
Year : 2007  |  Volume : 39  |  Issue : 1  |  Page : 33-38

Antioxidant activity of ethyl acetate soluble fraction of Acacia arabica bark in rats


R and D Center, The Himalaya Drug Company, Bangalore-562 123, India

Correspondence Address:
S K Mitra
R and D Center, The Himalaya Drug Company, Bangalore-562 123
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0253-7613.30761

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Objective: To study the antioxidant activity of various extracts and fractions of Acacia arabica by in vitro and in vivo experimental models. Materials and Methods: Various solvent extracts were prepared by Soxhlet extraction. Extract fractionations were done by solvent-solvent extraction and flash chromatographic separation. In vitro lipid peroxidation was carried out by tertiary butyl hydroperoxide -induced lipid peroxidation. The most active fractions were identified and standardized by thin layer chromatography (TLC). In vivo experiments on the most active fraction were carried out with 50, 100, and 150 mg/kg, p.o. doses, in carbon tetrachloride (CCl 4 )-induced hepatotoxicity, in rats. Various biochemical parameters like serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT), superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), glutathione (GSH), and lipid peroxidation were estimated. Results: Flash chromatographic fractions 2-6 of ethyl acetate extract exhibited maximum activity with in vitro lipid peroxidation. In vivo evaluation of this active fraction (AA) in CCl4-induced hepatotoxicity for 19 days at a dose of 150 mg/kg offered marked liver protection, which was evident by significant changes in lipid peroxidation, glutathione, superoxide dismutase and catalase ( P <0.01). The treatment also showed significant changes in AST, ALT, and GSH-Px levels ( P <0.05). At lower doses, the protection was not consistent. Conclusion: The polyphenol rich active fraction of Acacia arabica is a potent free radical scavenger and hepatoprotective and protects TBH-induced lipid peroxidation and CCl 4 -induced hepatic damage.






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