title: [The cardioprotective effects of ischemic postconditioning on myocardial interstitium following ischemic/reperfusion in rats].
abstract: OBJECTIVE
  To investigate the effects of ischemic postconditioning (IPTC) on the changes of matrix metalloproteinases-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) protein and mRNA levels in rat heart subjected to ischemia/reperfusion, and explore the mechanism by which IPTC protects myocardial interstitium following ischemic/reperfusion (I/R).
  
  
  METHODS
  Twenty four healthy male SD rats were randomly divided into 3 groups (n = 8): sham control (SC) group, I/R group and IPTC group. The parameters of left ventricular function including left ventricular systolic pressure (LVSP) and its derivate (±dp/dt) were measured; the amount of myocardial collagen contents was determined by hydroxyproline quantification; the plasma activity of creatine kinase (CK) and lactate dehydrogenase (LDH) was detected; the protien levels of MMP-2 and TIMP-2 was measured by Western blot and the mRNA levels of MMP-2 and TIMP-2 was detected by real-time PCR.
  
  
  RESULTS
  The myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were significantly decreased in I/R group compared with those of SC group, wherease the activities of CK and LDH in the plasma and the protein and mRNA levels of MMP-2 were significantly enhanced in I/R group when compared to SC group. Compared with I/R group, the myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were increased in IPTC group, the activities of CK and LDH in the plasma and the protein and mRNA level of MMP-2 were decreased in IPTC group.
  
  
  CONCLUSIONS
  These findings indicate that IPTC has protective effects on myocardial interstitial after the myocardial ischemia/reperfusion injury, and IPTC may exert its cardioprotectve effect via inhibiting MMP-2 and enhancing TIMP-2 expression in cardiac muscle.
authors.affiliation: Department of Pathophysiology, Changzi Medical College, China.
authors.forename: Yan-Zhen
authors.initials: YZ
authors.lastname: Lu
authors.forename: Jia
authors.initials: J
authors.lastname: Wang
authors.forename: Cui-Ying
authors.initials: CY
authors.lastname: Zhang
authors.forename: Juan
authors.initials: J
authors.lastname: Song
authors.forename: Bao-Hong
authors.initials: BH
authors.lastname: Li
authors.forename: Xiao-Liang
authors.initials: XL
authors.lastname: Song
mesh_terms: D000818:Animals; D003094:Collagen / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D057775:Ischemic Postconditioning; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism; D016277:Ventricular Function, Left
chemical_list: D019716:Tissue Inhibitor of Metalloproteinase-2; D003094:Collagen; D003402:Creatine Kinase; D020778:Matrix Metalloproteinase 2; C522363:Mmp2 protein, rat