摘要
脑缺血-再灌注损伤是一个复杂的级联反应过程,涉及多种机制,其中氧化应激起到关键作用。目前的研究表明,氧化应激可以通过脂质过氧化、蛋白质变性和/或DNA修饰等途径促使神经细胞坏死,也可以通过线粒体、内质网或死亡受体等途径启动神经细胞凋亡。本文就氧化应激在脑缺血-再灌注损伤中的作用机制及抗氧化治疗的新进展作一综述。
Cerebral ischemia-reperfusion injury is a complex cascade of reactions involving a variety of mechanisms,among which oxidative stress plays a key role.Recent studies suggest that oxidative stress may promote neuronal necrosis via lipid peroxidation,protein degeneration,and/or DNA modification.Oxidative stress can also trigger neuronal apoptosis through the mitochondrial pathway,the endoplasmic reticulum pathway,or the death receptor pathway.This review focuses on the mechanisms of oxidative stress during cerebral ischemia-reperfusion injury and the progress made in its treatment with antioxidants.
出处
《国际病理科学与临床杂志》
CAS
2012年第4期343-346,共4页
Journal of International Pathology and Clinical Medicine
基金
中南大学大学生创新训练项目(CL11251)~~
关键词
脑缺血-再灌注损伤
氧化应激
抗氧化治疗
cerebral ischemia-reperfusion injury； oxidative stress； antioxidant treatment
