脑缺血再灌注损伤中凋亡调控基因表达的变化及意义  

Change of Apoptosis Controlling Gene in Cerebral Ischemia Reperfusion Injury and Its Significance

作　　者：于志君[1] 成彩莲[1] 

机构地区：[1]武汉科技大学医学院,湖北武汉430080

出　　处：《武汉科技大学学报》2006年第4期425-428,共4页Journal of Wuhan University of Science and Technology

摘　　要：脑缺血再灌注损伤的病理机制十分复杂,目前许多学者发现细胞凋亡与其密切相关。细胞凋亡是一种基因控制的细胞主动死亡,它参与机体许多病理生理过程。研究资料表明,脑缺血再灌注损伤是诱导凋亡调控基因表达的最强烈刺激之一。脑缺血再灌注后,有多种基因被诱导表达,这些基因编码的蛋白质产物直接或间接参与了凋亡的调控。对脑缺血再灌注后的bc l-2基因家族、fas基因、p53基因的表达及作用机制进行论述。Cerebral ischemical reperfusion injury is very complicated and closely related with apoptosis according to many researches. Apoptosis, an initiative death of cell, is a part of many pathoprocess and physio-process. Most researches indicate that cerebral ischemical reperfusion injury is one of the most intense motivations. Many genes are expressed following cerebral ischemical reperfusion injury and their coding proteins are correlated with apoptosis regulation directly or indirectly. This article reviews gene （bcl-2, fas, p53） expression and mechanism of action after cerebral ischemical reperfusion injury.

关 键 词：脑缺血 再灌注 凋亡 

分 类 号：R364.17[医药卫生—病理学]