当前位置： SCI文献检索 > JOURNAL OF PHARMACOLOGICAL SCIENCES期刊下所有文献 > Ameliorative effects of tannic acid on carbon tetrachloride-induced liver fibrosis in vivo and in vitro.

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

Abstract：

: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.

journal_name

J Pharmacol Sci

journal_title

Journal of pharmacological sciences

authors

Chu X,Wang H,Jiang YM,Zhang YY,Bao YF,Zhang X,Zhang JP,Guo H,Yang F,Luan YC,Dong YS

doi

10.1016/j.jphs.2015.12.002

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

15-23

issue

1

eissn

1347-8613

issn

1347-8648

pii

S1347-8613(15)00242-X

journal_volume

130

pub_type

杂志文章

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