Abstract:AimTo observe whether rosuvastatin postconditioning (RPO) and ischemic postconditioning (IPO) could attenuate ischemia-reperfusion injury (IRI) in T2DM rats, and to investigate the potential cardioprotective mechanisms involved.MethodsInduced by streptozotocin plus nicotinamide, a T2DM rat model was successfully created in 54 healthy Wistar male rats, which were randomly allocated into seven groups (n=9): Sham group, IRI group, RPO+IPO group, 5-HD group, diazoxide group, HMR-1098 group, and Cromakalim group.Infarct size, ultrastructure, serum cTnT were determined at the end of ischemia-reperfusion, which underwent 45 min ischemia and 120 min reperfusion.ResultsCompared with IRI group, the myocardial infarct size significantly decreased in RPO+IPO group and diazoxide group, HMR-1098 group, Cromakalim group (p<0.05).The myocardial infarct size in 5-HD group significantly increased than that in RPO group and diazoxide group, HMR-1098 group, and Cromakalim group (p<0.05).TEM revealed that the myocardial cell mitochondria ultrastmctural damages were serious in IRI group and 5-HD group.In RPO+IPO group, diazoxide group, HMR-1098 group and Cromakalim group, the structure of most mitochondria maintained as originally on the whole.As compared with IRI group, the level of cTnT in RPO+IPO group and diazoxide group, HMR-1098 group, Cromakalim group was significantly reduced (p<0.05).The level of cTnT in 5-HD group was significantly increased than that in RPO+IPO group and diazoxide group, HMR-1098 group, Cromakalim group (p<0.05).ConclusionsRPO+IPO could significantly attenuate IRI in vivo T2DM rats.mitoKATP channel but not sarcKATP channel plays the major role in the protection effects of rosuvastatin postconditioning.
