Role of IPC and valsartan in myocardial ischemia reperfusion injury

AIM To study the relationship between ischemia precondition (IPC)/valsartan and signal transducer and activator of transcription 3 (STAT3) in ischemia-reperfusion (I/R) injury and to explore their role in myocardial protection. METHODS Thirty-two healthy male Wistar rats were randomly divided into four groups (I/R, IPC, VIR and VIPC groups). I/R and IPC were induced by intragastric administration with isotonic Na chloride for 1 week, and then I/R was subjected to 30 min of sustained ischemia by occluding the left anterior descending coronary artery (LAD) and 1 hour of reperfusion. IPC underwent 3 cycles of 5-minute occlusion and reperfusion of LAD before the experiment continued as I/R. VIR and VIPC were induced by intragastric administration with valsartan for 1 week (30 mg/kg), and then VIR continued as I/R, and VIPC continued as IPC. The pectoral cavity was opened to take blood from the right cardiac ventricle. Blood was centrifugated and serum was obtained to detect IL-6 by ELISA. Myocardial tissues in infarcted domain were obtained to detect phosphorylation of STAT3 by immunohistochemistry. RESULTS The phosphorylation of STAT3 was increased and the expression of IL-6 was degraded in IPC group compared to those in I/R group (P<0.01). The phosphorylation of STAT3 and the expression of IL-6 both were downregulated in Valsartan group compared to those in normal saline group (P<0.01). CONCLUSION Valsartan inhibits the reaction of inflammation, when myocardium is undergoing ischemia-reperfusion injury. IPC activates survival signaling of the myocardium by the phosphorylation of STAT3 and inhibits the reaction of myocardial inflammation. Valsartan can partly inhibit the activation of STAT3, and produce the role of myocardial protection.