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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.