Ameliorative effects of tannic acid on carbon tetrachloride-induced liver fibrosis in vivo and in vitro

We investigated the ameliorative effects and potential mechanisms of tannic acid (ta) in carbon tetrachloride (ccl4)-intoxicated mice and hepatic stellate cells (hscs). liver fibrosis was observed in ccl4 (800 ml/kg)-induced mice,and high viability was observed in ccl4 (10 mm)-intoxicated hscs. pre-treatment of mice with ta (25 or 50 g/kg/day) significantly ameliorated hepatic morphology and coefficient values and reduced the activities of aspartate aminotransferase (ast) and alanine aminotransferase (alt),the concentrations of malondialdehyde (mda) and serum levels of endothelin-1 (et-1). in addition,ta increased the activities of superoxide dismutase (sod),catalase (cat),glutathione peroxidase (gsh-px),and endothelial nitric oxide synthase (enos) and the serum level of no. moreover,ta reduced the expression of angiotensin ii receptor-1 (atr-1),interleukin-1β (il-1β),tumor necrosis factor-α (tnf-α),transforming growth factor-β (tgf-β),caspase-3,c-fos,c-jun,the ratio of bax/bcl-2,tissue inhibitor of metalloproteinase-1 (timp-1) and ta increased matrix metal proteinase-9 (mmp-9),matrix metalloproteinase-1 (mmp-1). furthermore,ta (0.01 μm,0.1 μm or 1 μm) decreased the timp-1/mmp-1 ratio and reduced the viability of hscs. these results indicated that ta exerts significant liver-protective effects in mice with ccl4-induced liver fibrosis. the potential mechanism may rely on the inhibition of collagen accumulation,oxidative stress,inflammation and apoptosis. © 2015 japanese pharmacological society.