title: [Antagonistic effect and mechanism of Rosuvastatin on myocardial apoptosis in rats with acute myocardial infarction].
abstract: OBJECTIVE
  To investigate the protective effect of Rosuvastatin on myocardial cells in rats with acute myocardial infarction and its possible mechanism.
  
  
  METHODS
  Rats were randomly assigned to four groups: Control group, Sham group, AMI and Rosuvastatin group. The levels of lactate dehydrogenase (LDH) and creatine jubase (CK), the vitality of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were detected by assay kits and the levels of C-reactive protein (CRP), tumor necrosis factor (TNF) alpha and interleukin (IL)-6 expression were detected by enzyme linked immunosorbent assay (ELISA). TTC/Evans blue staining was used to determine the relative myocardial infarction area, HE staining was used to detect pathologic changes and myocardial apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL). What's more, Western blot was used to detect the protein expression of B-cell lymphoma-2 (Bcl-2), Bax, cleaved-Caspase-3, Rock1, Rock2, I-κB and NF-κBp65.
  
  
  RESULTS
  The model of acute myocardial infarction rats was established. Compared with Sham group, the myocardial pathological changes were more severe, and the apoptosis number, the production of inflammatory factors and oxidative damage were significantly increased in AMI group. Compared with AMI group, the relative area of infarction myocardium (43% ± 4% vs 31% ± 8%, P=0.004 3) was dramatically reduced, the levels of LDH (2 545.45 ± 613.67 U/L vs 1 573.43 ± 373.72 U/L, P=0.02) and CK (7.49 ± 1.75 U/ml vs 4.42 ± 1.28 U/ml, P=0.04) in serum were significantly lower (P<0.01), the myocardial pathological damage degree was relieved, the apoptosis number (41% ± 8% vs 23% ± 6%, P=0.014 7) was significantly decreased, the expression of Bax (1.17 ± 0.10 vs 0.57 ± 0.08, P=0.003) and cleaved-Caspase-3 (1.31 ± 0.07 vs 0.70 ± 0.01, P=0.004) were dramatically reduced, and the expression of Bcl-2 (0.19 ± 0.01 vs 0.32 ± 0.01, P=0.003) was enhanced in Rosuvastatin group. Furthermore, the production of inflammatory factors and oxidative damage were effectively alleviated (P<0.05), the protein expression of Rock1, Rock2 and NF-κBp65 were declined in Rosuvastatin group (P<0.01).
  
  
  CONCLUSIONS
  Rosuvastatin can effectively alleviate the cardiomyocyte apoptosis induced by acute ischemia, and its main mechanism may be the inhibition on RhoA/ROCK activation and the oxidative stress and inflammation reaction mediated by it.
authors: Department of Cardiology, Central Hospital of Fushun, Fushun 113006, China; Email: szcclszccl@163.com.
authors: Zhanchun
authors: Z
authors: Song
authors: Jinghui
authors: J
authors: Bai
authors: Qi
authors: Q
authors: Wang
authors: Liang
authors: L
authors: Chen
authors: Qunping
authors: Q
authors: Guo
authors: Di
authors: D
authors: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002097:C-Reactive Protein; D053148:Caspase 3; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase; D009203:Myocardial Infarction; D009206:Myocardium; D018384:Oxidative Stress; D051381:Rats; D000068718:Rosuvastatin Calcium; D013482:Superoxide Dismutase; D014409:Tumor Necrosis Factor-alpha
chemical_list: D007527:Isoenzymes; D014409:Tumor Necrosis Factor-alpha; D000068718:Rosuvastatin Calcium; D002097:C-Reactive Protein; D007770:L-Lactate Dehydrogenase; C409676:lactate dehydrogenase 2; D013482:Superoxide Dismutase; C505410:Casp3 protein, rat; D053148:Caspase 3