DAA-I inhibits ischemia/reperfusion injury induced apoptosis of cardiac microvascular endothelial cell through attenuating endoplasimic reticulum stress
Background Acute reperfusion of the jeopardized myocardium results in a cascade of harmful events, referred to as reperfusion injury.Factors contributing to reperfusion injury include cardiomyocytes and endothelial cell dysfunction or apoptosis.Recently, we and other groups found that cardiac microvascular endothelial cells (CMECs) also play an important role during I/RI of heart.In I/R myocardium, sudden increase of oxygen free radicals and other stimulus can potentially induce endoplasmic reticulum stress (ERS)-initiated apoptotic signaling.Previous study showed that the cardioprotective effect accorded by des-aspartate-angiotensin Ⅰ (DAA-Ⅰ) was the result of its anti-inflammatory actions on early inflammatory processes in myocardial ischemia-reperfusion injury.However, it has not been established that whether DAA-Ⅰ could protect CMECs against I/R injury and whether ERS phenomenon is involved.In our study, we explore the protective effect and possible mechanism of DAA-I against I/RI of cardiac microvascular endothelial cell.
DANG Jing-yi SI Rui GUO Wen-yi
Department of Cardiology,Xijing Hospital,Fourth Military Medical University,Xi”an,China
国内会议
北京
英文
115-116
2013-03-20(万方平台首次上网日期,不代表论文的发表时间)