naling pathway on the aspect of inhibiting MMECs apoptosis to explore mechanisms of reduced myocardial ischemia-reper- fusion injury due to opening of mito-KATP. MATERIAL AND METHODS Culture and identification of MMECs

and it is an important factor that leading to cardiac ischemiareperfusion injury. In the past, most attention was focused on cardiac cells. While in recent years, myocardiac microvascular endothelial cells (MMECs) attracted scholar’s attention. The one hand, endothelial cells participate in many important body balance regulation, and can synthesize and secrete a variety of biologically active substances, the other hand they regulate blood coagulation, leukocyte activity and the platelet aggregation and may be the first spreading site of reperfusion injury (1, 2). Anti-apoptotic mechanism for cell protection on reperfusion may provide a new method to reduce reperfusion injury. Papers have reported that PI3K/Akt signaling and mitochondrial ATP sensitive potassium channel (Mito-KATP) have protective effect on the heart, brain, blood vessels, and they may play important roles in endothelial cells, such as angiogenesis, proliferation, microvascular permeability, etc (3-6). In this study, we chose MMECs as the research object, and made hypoxia/ reoxygen (H/R) model to imitate ischemia-reperfusion injury, pretreated with diazoxide (DZ) to open mito-KATP, observed the effect of PI3K/Akt signaling pathway on the aspect of inhibiting MMECs apoptosis to explore mechanisms of reduced myocardial ischemia-reperfusion injury due to opening of mito-KATP.