Berbamine ameliorates ethanol-induced liver injury by inhibition of hepatic inflammation in mice  

作　　者：LIU Xin-Yu CHEN Guan-Nan DU Guo-Ming PAN Yue SONG Wu-Qi JIANG Ting-Wang LIU Hai-Liang 

机构地区：[1]Department of Microbiology,Wu Lien-Teh Institute,Harbin Medical University,Harbin 150081,China [2]Department of Key Laboratory,The Second People’s Hospital of Changshu,The Affiliated Changshu Hospital of Xuzhou Medical University,Changshu 215500,China

出　　处：《Chinese Journal of Natural Medicines》2020年第3期186-195,共10页中国天然药物（英文版）

基　　金：National Natural Science Foundation of China(NSFC)(No.81701573);Key Technologies of Prevention and Control for Major and Infectious Diseases Project of Suzhou(No.GWZX201604);Youth Medical Talent Project of Jiangsu(No.QNRC2016214)。

摘　　要：Alcoholic liver disease(ALD) has become one of the leading causes of death in the world. Berbamine(BM), a natural product mainly derived from Berberis vulgaris L, possesses multiple bioactivities as a traditional medicine. However, the protective effect of BM on ALD remains unknown. In this study, we investigated the effect of BM on ethanol-induced hepatic injury in mice and its underlying mechanism. It was shown that BM at 0.3125-40 μmol·L^-1 had no effect on macrophages and hepatocytes proliferation. BM at 5-20 μmol·L^-1 significantly inhibited lipopolysaccharide(LPS) or acetate-induced IL-1β and IL-6 m RNA expression in RAW264.7 cells. Moreover, BM treatment significantly inhibited LPS-induced p65 and STAT3 phosphorylation in RAW264.7 cells. Hepatic histopathology analysis showed that inflammatory cells infiltration and lipid accumulation were suppressed by 25 and 50 mg·kg^-1 BM administration in ethanol-induced hepatic injury mouse model. Meanwhile, BM treatment significantly inhibited serum ALT and AST levels in ethanol-fed mice. Oil red O staining results showed that BM administration ameliorated hepatic lipid accumulation in ethanolfed mice. Preventions of ethanol-induced hepatic injury by BM were reflected by markedly decreased serum and hepatic triglyceride(TG) and total cholesterol(TC) contents. Real-time PCR results showed that BM treatment significantly inhibited pro-inflammatory cytokines m RNA expression in ethanol-fed mouse liver. Remarkably, the mechanism of action of BM was related to the reduction of ethanol-induced NF-κB and STAT3 phosphorylation levels in liver. In addition, BM treatment significantly inhibited ERK phosphorylation but not JNK and p38 of MAPK pathway. Taken together, our results demonstrate a beneficial effect of BM on ethanol-induced liver injury via a mechanism associated with inactivation of NF-κB, STAT3 and ERK pathway, which gives insight into the further evaluation of the therapeutic potential of BM for ALD.

关 键 词：BERBAMINE ETHANOL HEPATIC INJURY NF-κB INFLAMMATION 

分 类 号：R965[医药卫生—药理学]