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

作者机构：Department of MicrobiologyWu Lien-Teh InstituteHarbin Medical UniversityHarbin 150081China Department of Key LaboratoryThe Second People’s Hospital of ChangshuThe Affiliated Changshu Hospital of Xuzhou Medical UniversityChangshu 215500China 

出 版 物：《Chinese Journal of Natural Medicines》 (中国天然药物（英文版）)

年 卷 期：2020年第18卷第3期

页      面：186-195页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 1005[医学-中医学] 100706[医学-药理学] 1002[医学-临床医学] 0703[理学-化学] 100602[医学-中西医结合临床] 10[医学] 

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) 

主　　题：Berbamine Ethanol Hepatic injury NF-κB Inflammation 

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.