OBJECTIVE: to investigate the combined effect of rosuvastatin (RSV) and ischemic postconditioning (PC) on myocardial ischemia-reperfusion (I/R) injury in a type 2 diabetic rat model. METHODS: type 2 diabetic (induced by streptozotocin plus nicotinamide) rats, undergoing 30 min ischemia and 120 min reperfusion, were divided into six groups (n = 10 each): Sham, I/R without other interventions, RSV before reperfusion, PC with 3 cycles of 10 s reperfusion and 10 s ischemia, RSV + PC and RSV + PC + PI3-K inhibitor LY294002. Myocardial infarct size (IS), ultrastructural change and myocardial expression of phosphorylated eNOS/total eNOS were determined. RESULTS: IS and ultrastructural damages were all significantly reduced and myocardial eNOS phosphorylation was significantly increased in RSV and PC groups compared with the I/R group (all P < 0.05) these beneficial effects were further enhanced by RSV + PC (all P < 0.05 vs. RSV and PC, respectively). The beneficial effects were significantly attenuated by PI3K inhibitor LY294002. CONCLUSIONS: the results indicate that RSV + PC could alleviate myocardial ischemia-reperfusion injury in this type 2 diabetic model by activating PI3K/AKT/eNOS signaling pathway.
OBJECTIVE: to investigate the combined effect of rosuvastatin (RSV) and ischemic postconditioning (PC) on myocardial ischemia-reperfusion (I/R) injury in a type 2 diabeticrat model. METHODS: type 2 diabetic (induced by streptozotocin plus nicotinamide) rats, undergoing 30 min ischemia and 120 min reperfusion, were divided into six groups (n = 10 each): Sham, I/R without other interventions, RSV before reperfusion, PC with 3 cycles of 10 s reperfusion and 10 s ischemia, RSV + PC and RSV + PC + PI3-K inhibitor LY294002. Myocardial infarct size (IS), ultrastructural change and myocardial expression of phosphorylated eNOS/total eNOS were determined. RESULTS: IS and ultrastructural damages were all significantly reduced and myocardial eNOS phosphorylation was significantly increased in RSV and PC groups compared with the I/R group (all P < 0.05) these beneficial effects were further enhanced by RSV + PC (all P < 0.05 vs. RSV and PC, respectively). The beneficial effects were significantly attenuated by PI3K inhibitor LY294002. CONCLUSIONS: the results indicate that RSV + PC could alleviate myocardial ischemia-reperfusion injury in this type 2 diabetic model by activating PI3K/AKT/eNOS signaling pathway.