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

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• 作者：Xi Chu^a ; ^{chux2014@126.com" class="auth_mail" title="E-mail the corresponding author} ; Hua Wang^b ; Yan-min Jiang^c ; Yuan-yuan Zhang^d ; ^e ; Yi-fan Bao^f ; Xuan Zhang^d ; ^e ; Jian-ping Zhang^d ; ^e ; Hui Guo^d ; Fan Yang^d ; Yan-chao Luan^g ; Yong-sheng Dong^h
• 关键词：Tannic acid ; Anti-fibrosis ; Anti-oxidation ; Anti-Inflammation ; Anti-Apoptosis
• 刊名：Journal of Pharmacological Sciences
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：130
• 期：1
• 页码：15-23
• 全文大小：5160 K

文摘

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.