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Sophocarpine alleviates non‐alcoholic steatohepatitis in rats
Author(s) -
Song ChunYan,
Zeng Xin,
Chen SiWen,
Hu PingFang,
Zheng ZhiWu,
Ning BeiFang,
Shi Jian,
Xie WeiFen,
Chen YueXiang
Publication year - 2011
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2010.06561.x
Subject(s) - steatohepatitis , medicine , adiponectin , endocrinology , fibrosis , fatty liver , steatosis , aspartate transaminase , alanine transaminase , liver injury , insulin resistance , disease , biology , biochemistry , obesity , alkaline phosphatase , enzyme
Background and Aim: Non‐alcoholic steatohepatitis (NASH) is one entity in the spectrum of non‐alcoholic fatty liver disease (NAFLD). The aim of this study was to explore the prevention and therapeutic effect of sophocarpine on experimental rat NASH. Methods: Sophocarpine with the dosage of 20 mg/kg/day was injected into NASH rats. At the end of 12 weeks, all rats were killed to detect the degree of fatty degeneration, inflammation and fibrosis. Results: Sophocarpine intervention (in the pro‐treated and treated groups) resulted in a significant decrease of liver weight, liver index, serum transaminase and serum lipids. Messenger RNA expressions of leptin, interleukin (IL)‐6, tumor necrosis factor (TNF)‐α, transforming growth factor (TGF)‐β1, procollagen‐I and α‐smooth muscle actin (SMA) and deposition of IL‐6, TNF‐α and TGF‐β1 in liver decreased, whereas the messenger RNA expression of adiponectin increased significantly compared with that in the model group. Moreover, histological improvement was also observed in the sophocarpine intervention group. In addition, there was no significant difference in any detected indicator between the pro‐treated and treated group. Conclusions: Sophocarpine could decrease the level of serum transaminase, improve lipid metabolism, reduce synthesis of inflammatory cytokines TNF‐α, TGF‐β1 and IL‐6, activate protective adipocytokine adiponectin, and might be selected as a promising agent for the clinical prevention and therapy of NASH.