Hepatoprotection by Ginsenoside Rg1 in alcoholic liver disease

作者全名："Yang, Cheng; He, Xiaoqing; Zhao, Jinqiu; Huang, Wenxiang"

作者地址："[Yang, Cheng; He, Xiaoqing; Zhao, Jinqiu; Huang, Wenxiang] Chongqing Med Univ, Dept Infect Dis, Affiliated Hosp 1, Chongqing 400016, Peoples R China; [He, Xiaoqing] Chongqing Publ Hlth Med Ctr, Div Infect Dis, Chongqing 400036, Peoples R China"

通信作者："Zhao, JQ; Huang, WX (corresponding author), Chongqing Med Univ, Dept Infect Dis, Affiliated Hosp 1, Chongqing 400016, Peoples R China."

来源：INTERNATIONAL IMMUNOPHARMACOLOGY

ESI学科分类：PHARMACOLOGY & TOXICOLOGY

WOS号：WOS:000659468200003

JCR分区：Q1

影响因子：5.6

年份：2021

卷号：92

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Ginsenoside Rg1; Alcoholic hepatitis; CYP2E1; NLRP3

摘要："Alcoholic hepatitis (AH) has caused serious mortality to the world's population. Despite tremendous efforts to reduce disease burden, effective treatments for this disease are still lacking. Ginsenoside Rg1 (G-Rg1) has been reported to be hepatoprotective in several liver injury models. However, therapeutic potential of this drug in AH has not been tested. In this study, using a chronic ethanol-feeding model, we found that ethanol-fed mice presented clinical indicators of liver injury, such as elevated serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST) and total bilirubin (Tbil), as well as development of hepatic steatosis. Upon treatment with G-Rg1, animals showed marked decreases in serum biochemical parameters, as well as improvement in liver histology. Mechanistically, G-Rg1 blocked the induction of cytochrome P4502E1 (CYP2E1), and prevented the generation of reactive oxygen species (ROS), mitochondria damage, as well as hepatocellular apoptosis. As a result, NLRP3 inflammasome activation was inhibited, which subsequently suppressed the production of active caspase-1 and inflammatory cytokines. Our data has demonstrated a hepatoprotective role for G-Rg1 in AH, and identified potential drugable pathways to improve disease outcomes. These findings may have significant implications for developing novel therapies for inflammatory liver diseases."

基金机构："Chongqing Yuzhong Science and Technology Commission [20200119]; Chongqing Natural Science FoundationNatural Science Foundation of Chongqing [cstc2020jcyj-msxmX0159, cstc2020jcyj-msxmX0281, cstc2020jcyj-msxmX0224]; First Affiliated Hospital of Chongqing Medical University [PYJJ2019-06]; Chongqing Medical Science Project [2018MSXM065, 2020FYYF008]; Chongqing Education Commission [KJQN201900449]"

基金资助正文："This work received support from Chongqing Yuzhong Science and Technology Commission (20200119), Chongqing Natural Science Foundation (cstc2020jcyj-msxmX0159, cstc2020jcyj-msxmX0281 and cstc2020jcyj-msxmX0224), The First Affiliated Hospital of Chongqing Medical University (PYJJ2019-06), Chongqing Medical Science Project (2018MSXM065, 2020FYYF008) and Chongqing Education Commission (KJQN201900449). We thank Dr. Luis J. Cocka (Department of Microbiology, Perelman School of Medicine at University of Pennsylvania) for helping to proof read of this manuscript."