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KMID : 1134820100390030343
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Journal of the Korean Society of Food Science and Nutrition
2010 Volume.39 No. 3 p.343 ~ p.349
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Effects of Green Tea Extract on Acute Ethanol-induced Hepatotoxicity in Rats
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Jin Dong-Chun
Jeong Seung-Wook
Park Pyoung-Sim
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Abstract
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The liver is the major target of ethanol toxicity and oxidative stress plays a role in development of alcoholic liver disease. This study was performed to investigate the effects of green tea extracts (GTE) on acute ethanol-induced hepatotoxicity in rats. Experimental animals were divided into 4 groups, control, GTE, ethanol, and GTE＋ethanol treatment, with 5 rats in each group. Ethanol (6 g/kg body weight (BW)) and GTE (200 mg/kg BW) were treated by gavage. At 1 hour, 3 hours and 20 days (6 g/kg BW every 2 days for total 10 doses) after ethanol and/or GTE treatments, animals were killed; hepatic tumor necrosis factor-alpha (TNF-α) and glutathione level, serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT), hepatic antioxidant enzymes (SOD, CAT, GPx) activities and hepatic thiobarbituric acid reactive substances (TBARS) were measured. At 1 hour and 3 hours, hepatic TNF-α levels were increased significantly in ethanol group and ethanol＋GTE group but that levels was significantly lower in ethanol＋GTE group compared with ethanol group. Hepatic glutathione level was decreased by ethanol treatment but GTE prevented the ethanol-induced glutathione decrement. The levels of liver marker enzymes (AST, ALT), liver antioxidant enzymes (SOD, CAT, GPx) and lipid peroxidation marker (TBARS) were not changed in rats of 1 and 3 hours after ethanol treatment. After 20 days, GTE decreased the changes of liver marker enzymes (AST, ALT) activities and TBARS level by ethanol. This study shows that GTE beneficially modulates TNF-α and glutathione levels in liver of ethanol administered rats. The GTE supplementation could be beneficial to liver by decreasing early changes of biomarkers of liver damage caused by ethanol.
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KEYWORD
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green tea extract, ethanol, TNF-α, hepatotoxicity, glutathione
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