氧化应激在脑缺血损伤中的作用机制  

Mechanisms of Oxidative Stress in Brain Ischemia Injury

作　　者：赵丹洋[1] 吴伟康[1] 

机构地区：[1]中山大学中山医学院病理生理教研室,广州510080

出　　处：《中山大学研究生学刊（自然科学与医学版）》2003年第4期13-19,共7页Journal of the Graduates Sun YAT-SEN University(Natural Sciences.Medicine)

摘　　要：脑缺血是一个复杂的损伤级联反应,其中氧化应激损伤起了关键的作用。氧化应激产生的氧化产物不但可以直接攻击大分子物质如脂肪、蛋白、核酸,使之发生过氧化,导致细胞坏死,还可以通过间接介导线粒体途径、DNA修复酶及转录因子等导致细胞凋亡。通过应用抗氧化酶(如超氧化物歧化酶等),可以有效防止氧化损伤、阻断氧化应激在脑缺血后的信号传导和损伤。本文就氧化应激在脑缺血损伤中的作用机制作一综述。Oxidative stress has been implicated in brain injury after ischemia, which is a complex cascade. These oxidants produced by oxidative stress are directly involved in oxidative damage with cellular macromolecules such as lipids, proteins and nucleic acids, which lead to cell death. Oxidants are also mediators in signaling involving mitochondria pathway, DNA repair enzymes, and transcription factor that may lead to apoptosis after cerebral ischemia. antioxidangt enzymes (such as superoxide dismutase, etc) provide useful tools in dissecting the events involving oxidative stress in signaling and damage in ischemic brain injury. This review focuses on the mechanisms of oxidative stress during brain ischemia.

关 键 词：氧化应激 脑缺血 损伤级联反应 氧化产物 DNA修复酶 转录因子 抗氧化酶 神经元损伤 超氧化物歧化酶 

分 类 号：R743.31[医药卫生—神经病学与精神病学] Q554.6[医药卫生—临床医学]