缺血预处理抗心肌细胞凋亡的相关基因调控机制的研究  

Study about Regulatory Mechanism of Related Gene of Anti-myocardial Apoptosis by Ischemic Preconditioning

作　　者：李上海[1] 梁伟钧[1] 

机构地区：[1]广东医学院附属医院心内科,广东湛江524023

出　　处：《医学综述》2007年第24期1957-1959,共3页Medical Recapitulate

基　　金：广东省科技计划项目(20052042178)

摘　　要：心肌缺血再灌注损伤可诱发心肌细胞凋亡,这可能与启动许多凋亡相关基因的表达发生改变有相关,如fas家族基因、Bcl家族基因、c-fos基因、c-jun基因、核因子κB等。而缺血预处理可以通过减少细胞凋亡来减轻心肌缺血再灌注损伤的程度,这可能是抑制相关凋亡基因有关。全面了解这些基因表达改变及其意义,对于揭示缺血预处理的分子机制,从而进一步探索治疗心肌缺血再灌注损伤的分子靶具有重要意义。Myocardial ischemia-reperfusion injury can result in myocardial apoptosis, which maybe cor-related with priming of expression changes of many apoptosis-reated genes, such as fas family gene, Bcl family gene, c-fos gene,c-jun gene, NK-tcB factory and so on. Isehemic preconditioning can reduce the degree of myocardial ischemia-reperfusion injury by decreasing cell a/xrptosis, which maybe related to the inhibition of related apoptotic gene. Whole recognition of these genes about expression changes and its significance will be helpful to further study the molecular target in treating myocardial ischemia-reperfusion injury.

关 键 词：心肌缺血再灌注损伤 细胞凋亡 缺血预处理 基因蛋白 

分 类 号：R541.4[医药卫生—心血管疾病]