Rosuvastatin enhances the protective effects of ischemic postconditioning on myocardial ischaemia-reperfusion injury in type 2 diabetic rat
10.3760/cma.j.issn.0253-3758.2010.09.013
- VernacularTitle:瑞舒伐他汀后处理联合缺血后处理减轻2型糖尿病大鼠心肌缺血再灌注损伤
- Author:
Wei CAI
1
;
Jun FANG
;
Zhao-Yang CHEN
;
Yun-Ling LIN
;
Li-Ming WU
;
Liang-Long CHEN
Author Information
1. 福建医科大学附属协和医院
- Keywords:
Myocardial reperfusion injury;
Diabetes mellitus,type 2;
Rosuvastatin
- From:
Chinese Journal of Cardiology
2010;38(9):814-818
- CountryChina
- Language:Chinese
-
Abstract:
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 L/R group (all P < 0. 05 ) these benefical 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.
