摘要
心肌缺血预适应及后适应作为机体的一种内源性保护,分别具有缺血/再灌注损伤保护和再灌注损伤保护功能,尤其是在再灌注期可能存在共同的作用机制,如减少氧自由基生成,激动腺苷受体,募集再灌注损伤营救激酶途径,激活线粒体ATP敏感性钾通道,抑制线粒体渗透性转换孔道开放等。这些共同靶点可以为研制抗再灌注损伤药物提供新的思路。
As a powerful endogenous protection,myocardial ischemic preconditioning and postconditioning have cardioprotection against ischemia reperfusion injury and cardiopretection against reperfusion injury respectively.They perhaps share some mechanisms during reperfusion,such as reduction of the production of oxygen free radical,activation of adenosine receptors,recruit of reperfusion injury salvage kinases,opening of the mitochondrial KATP channel,and inhibition of the mitochondrial permeability transition pore.These common targets may provide new strategy for development of drugs against reperfusion injury.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2007年第8期993-996,共4页
Chinese Pharmacological Bulletin
基金
天津市自然科学基金资助项目(No993608111)
关键词
再灌注
预适应
后适应
机制
reperfusion
preconditioning
postconditioning
mechanism