氧化应激在非酒精性脂肪性肝病发病机制中的作用研究进展  

Research Progress on the Role of Oxidative Stress in the Pathogenesis of Non-alcoholic Fatty Liver Disease

作　　者：陈金星 黄雅馨 俞昌喜[1,2] 岳荣彩 CHEN Jin-xing;HUANG Ya-xin;YU Chang-xi;YUE Rong-cai(Department of Pharmacology,School of Pharmacy,Fujian Medical University,Fuzhou 350122,China;Key Laboratory of Drug Target Discovery and Structural Function Research in Fujian Qrovince,Fuzhou 350122,China)

机构地区：[1]福建医科大学药学院药理学系,福建福州350122 [2]福建省药物靶点发现与结构功能研究重点实验室,福建福州350122

出　　处：《海峡药学》2024年第4期1-6,共6页Strait Pharmaceutical Journal

基　　金：国家自然科学基金项目(编号82000554);福建省自然科学基金项目(编号2023J0113)。

摘　　要：非酒精性脂肪性肝病(Non-alcoholic fatty liver disease,NAFLD)已成为全球范围内最常见的慢性肝病,并与氧化应激密切相关。脂质代谢紊乱导致肝脏脂质堆积,进而引起线粒体、内质网和其他氧化酶产生大量的活性氧(Reactive oxygen species,ROS)。ROS生成增加可引起胰岛素敏感性改变以及脂质代谢关键酶的表达和活性改变,但是氧化应激对NAFLD发病机制的作用尚不清楚。基于上述观点,本文综述了可能导致ROS过度产生的机制以及ROS驱动NAFLD进展的潜在机制。Non-alcoholic fatty liver disease(NAFLD) has become the most common chronic liver disease worldwide and is closely related to oxidative stress.Disorders of lipid metabolism lead to the accumulation of lipids in the liver,which in turn causes mitochondria,endoplasmic reticulum and other oxidases to produce large amounts of Reactive oxygen species(ROS).Increased ROS production can cause altered insulin sensitivity and altered expression and activity of key enzymes in lipid metabolism,but the role of oxidative stress on the pathogenesis of NAFLD is unclear.Based on the above viewpoints,this article reviews the mechanisms that may lead to the overproduction of ROS and the underlying mechanisms by which ROS drives the progression of NAFLD.

关 键 词：非酒精性脂肪性肝病 非酒精性脂肪性肝炎 活性氧 内质网 线粒体 氧化应激 脂质代谢 

分 类 号：R965[医药卫生—药理学]