海峡药学2024,Vol.36Issue(4) :1-6.

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

陈金星 黄雅馨 俞昌喜 岳荣彩
海峡药学2024,Vol.36Issue(4) :1-6.

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

陈金星 1黄雅馨 1俞昌喜 2岳荣彩2
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作者信息

  • 1. 福建医科大学药学院药理学系,福建福州 350122
  • 2. 福建医科大学药学院药理学系,福建福州 350122;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
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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.

Abstract

Non-alcoholic fatty liver disease(NAFLD)has become the most common chronic liver disease world-wide 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 Reac-tive 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 un-clear.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

Key words

Non-alcoholic fatty liver disease/Non-alcoholic steatohepatitis/Reactive oxygen species/Endoplasmic reticulum/Mito-chondria/Oxidative stress/Lipid metabolism

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基金项目

国家自然科学基金(82000554)

福建省自然科学基金(2023J0113)

出版年

2024
海峡药学
中国药学会福建分会

海峡药学

影响因子:0.643
ISSN:1006-3765
参考文献量69
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