title: Protective effects of fasudil hydrochloride post-conditioning on acute myocardial ischemia/reperfusion injury in rats.
abstract: BACKGROUND
  In recent years, the alleviation of acute myocardial ischemia and reperfusion injury (MI/RI) during myocardial reperfusion has presented a significant clinical challenge. This study was performed to investigate the effects of fasudil hydrochloride (FH) postconditioning on MI/RI and the underlying mechanism.
  
  
  METHODS
  Seventy-two rats were randomly divided into four groups: a Sham group, an ischemia/reperfusion (I/R) group, a fasudil hydrochloride (FH) group, and a fasudil hydrochloride+PI3K inhibitor (FH+I) group. Myocardial infarct size, cell apoptotic index (AI), and myocardial tissue expression of Rho-associated coiled-coil containing protein kinase 1 (ROCK1), Bcl-2, Bcl-2 associated X protein (Bax), caspase-3, Akt and phosphorylated Akt (P-Akt) were detected.
  
  
  RESULTS
  All these parameters, except Akt expression, were higher in the I/R group than in the Sham group (p < 0.05). Compared to the I/R group, myocardial infarct size, AI, Bax and caspase-3 expression were significantly reduced in the FH group (p < 0.05), while Bcl-2 expression was increased (p < 0.05). However, the myocardial infarct size and AI of the FH+I group were similar to those of the I/R group (p > 0.05). Compared to the FH group, Bcl-2 expression was reduced in the FH+I group, while Bax and caspase-3 expression was increased (p < 0.05). Furthermore, P-Akt expression in the FH group was significantly higher than that of the I/R group (p < 0.05).
  
  
  CONCLUSIONS
  FH post-conditioning alleviated MI/RI, with narrowing of the infarct size and decreased apoptosis of ischemic cardiocytes. The mechanism was associated with activation of the PI3K-Akt signaling pathway.
authors.affiliation: Department of Cardiology, No. 3 People's Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. zhangjf1222@yahoo.com.cn.
authors.forename: Zhi-hui
authors.initials: ZH
authors.lastname: Jiang
authors.forename: Tian-tian
authors.initials: TT
authors.lastname: Zhang
authors.forename: Jun-feng
authors.initials: JF
authors.lastname: Zhang
mesh_terms: D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D054460:rho-Associated Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: C494826:BAX protein, human; D047428:Protein Kinase Inhibitors; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D051057:Proto-Oncogene Proteins c-akt; C578418:ROCK1 protein, rat; D054460:rho-Associated Kinases; C505407:CASP3 protein, human; D053148:Caspase 3; C049347:fasudil