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- W2363761489 abstract "Aim To 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. Methods Induced 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. Results Compared with IRI group,the myocardial infarct size significantly decreased in RPO+IPO group and diazoxide group,HMR-1098 group,Cromakalim group(P0.05).The myocardial infarct size in 5-HD group significantly increased than that in RPO group and diazoxide group,HMR-1098 group,and Cromakalim group(P0.05).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,HMR1098 group,Cromakalim group was significantly reduced(P0.05).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(P0.05). Conclusions RPO+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." @default.
- W2363761489 created "2016-06-24" @default.
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- W2363761489 date "2012-01-01" @default.
- W2363761489 modified "2023-09-25" @default.
- W2363761489 title "Role of mitoK_(ATP) Channel in the Combination of Rosuvastatin and Ischemic Postcondition on Myocardium Against T2DM Rats Ischemia-Reperfusion Injury" @default.
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