缺血性脑血管病急性期氧化应激反应的机制研究  

Mechanism Study of Oxidative Stress in Acute Ischemic Cerebrovascular Disease

作　　者：唐明 安朋朋[2] 

机构地区：[1]青岛市海慈医疗集团神经内科,山东青岛266033 [2]山东中医药大学,济南250355

出　　处：《医学综述》2009年第22期3443-3445,共3页Medical Recapitulate

摘　　要：缺血性脑血管病的发病率逐年升高,其机制涉及众多。其中氧化应激损伤在脑缺血后神经细胞损伤中起了关键作用。氧化应激导致活性氧产生,直接损伤神经细胞,引发凋亡,激活一系列的损伤级联反应,涉及线粒体、Bcl家族、caspase以及钙蛋白酶等,并激活小神经胶质细胞的吞噬作用。对以上各种途径的深入研究,将为有效地防治缺血性脑血管病提供帮助。Ischemic cerebral vascular disease attacks more people in these years,but its mechanism remains unclear.Oxidative stress is believed to play a critical role in the ischemic cellular damage.The generation of reactive oxygen species in oxidative stress followed by apoptotic injury and pathways involves mitochondrial dysfunction,Bcl family,caspase and calpain activation,and microglial phagocytosis.With further insight into the cellular mechanisms of oxidative stress in ischemic cerebral vascular disease, it will be an efficient help to the clinical treatment.

关 键 词：缺血性脑血管病 氧化应激 活性氧 细胞凋亡 

分 类 号：R743.3[医药卫生—神经病学与精神病学]