title: [Rosuvastatin enhances the protective effects of ischemic postconditioning on myocardial ischaemia-reperfusion injury in type 2 diabetic rat].
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 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.
authors.affiliation: Department of Cardiology, Union Hospital, Fujian Medical University, Fujian Institute of Coronary Artery Disease, Fuzhou 350001, China.
authors.forename: Wei
authors.initials: W
authors.lastname: CAI
authors.forename: Jun
authors.initials: J
authors.lastname: FANG
authors.forename: Zhao-yang
authors.initials: ZY
authors.lastname: CHEN
authors.forename: Yun-ling
authors.initials: YL
authors.lastname: LIN
authors.forename: Li-ming
authors.initials: LM
authors.lastname: WU
authors.forename: Liang-long
authors.initials: LL
authors.lastname: CHEN
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications; D005464:Fluorobenzenes / Q000494:pharmacology*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D057775:Ischemic Postconditioning; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology / Q000648:ultrastructure; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011743:Pyrimidines / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D000068718:Rosuvastatin Calcium; D015398:Signal Transduction; D013449:Sulfonamides / Q000494:pharmacology*
chemical_list: D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt