Fruit extract of Paeonia anomala attenuates chronic alcohol-induced liver damage in rats

Fruit extract of Paeonia anomala attenuates chronic alcohol-induced liver damage in rats
사랑게렐윤지호강경수둘람자브 바슈렌직지드슈렌 툰삭노주원
Paeonia anomala; hepatoprotective; chronic alcohol; alanine aminotransferase; Mongolian
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Prolonged alcohol consumption develops alcoholic liver damage through generating reactive oxygen species, accumulating fatty acids and increasing inflammatory cytokines in liver. Paeonia anomala L. (Paeoniaceae) is used for treatment of many kinds of disorders in Mongolian traditional medicine using its fruit and root parts. In this study, hepatoprotective effect of fruit extract from P. anomala against chronic alcohol-induced liver damage was evaluated by measuring levels of liver damage marker enzymes (alanine aminotransferase and aspartate aminotransferase) in serum, and production of tumor necrosis factor alpha, triglyceride content, cytochrome P-450 2E1 enzyme induction, and endogenous anti-oxidative defenses including total glutathione, superoxide dismutase, glutathione peroxidase and glutathione reductase in liver. Spargue-Dawley rats were fed by Lieber DeCarli liquid diet for 5 weeks to develop alcohol-induced liver damage. Fruit extract of P. anomala (50 mg/kg body weight/day, 25 mg/kg body weight/day, and 10 mg/kg body weight/day) as well as reference control silymarin (25 mg/kg body weight/day) were administered along with the diet. Fruit extract of P. anomala protected the induction of alanine aminotransferase and aspartate aminotransferase in serum and attenuated the increased levels of triglyceride, tumor necrosis factor alpha, thiobarbituric acid reactive substances, and cytochrome P450 2E1 enzyme activity in liver comparing to those of ethanol-alone treated group. Anti-oxidative defenses such as total glutathione and glutathione peroxidase were increased in P. anomala group comparing to ethanol group. These results suggest that the fruit extract of P. anomala has hepatoprotective effect against chronic alcohol-induced liver damage via attenuating triglyceride accumulation and abnormal TNF-α production, and enhancing anti-oxidative defense mechanisms in liver.
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