国外心肌缺血/再灌注引发的细胞凋亡的治疗研究进展  

Progress on foreign research of treating on apotosis induced myocardial ischemia/reperfusion

作　　者：胡一冰[1] 林玉琳[2] 赵艳芝[2] 

机构地区：[1]首都医科大学燕京医学院临床医学系,2011级本科二班北京101300 [2]首都医科大学燕京医学院生理与病理生理教研室,北京101300

出　　处：《中国医药导报》2013年第5期32-34,共3页China Medical Herald

基　　金：首都医科大学教育提高质量项目(编号1000950306);首都医科大学校自然基金(编号2012ZR20)

摘　　要：心脏手术、急性心肌梗死溶栓等心肌缺血/再灌注可能造成缺血/再灌注损伤的发生,细胞凋亡是心肌缺血/再灌注损伤发生机制中的重要环节之一。通过有效物质抑制再灌注时诱发的细胞凋亡,可以减轻心肌缺血/再灌注损伤。心肌缺血/再灌注损伤引起细胞凋亡的途径是不同的,线粒体途径、死亡受体途径和内质网途径等是细胞凋亡信号转导的重要途径。本文以作用于缺血/再灌注损伤不同凋亡途径的有效物质作一综述。Ischamia/reperfusion, such as cardiosurgery, thrombolysis in myocardial infarction, etc, may result in is- chaemia reperfusion injury. Apoptosis is one of the important factors leading to the ischaemia/reperfusion injury. Apop- tosis inhibition by using effective substance could induce the injury during ischaemiaJreperfusion. Myocardial ischemi- a/reperfusion result apoptosis in different ways, mitochondrial pathway, death receptor pathway and endoplasmic retic- ulum pathway are the important pathways of signal transduction to apoptosis. This paper reviews and summarizes dif- ferent effective substances which reduce the damage of apoptosis according to these pathways

关 键 词：心肌 缺血 再灌注 凋亡 

分 类 号：R542.2[医药卫生—心血管疾病]