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1.
Chinese Journal of Applied Physiology ; (6): 431-435, 2014.
Article in Chinese | WPRIM | ID: wpr-243468

ABSTRACT

<p><b>OBJECTIVE</b>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).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>


Subject(s)
Animals , Male , Rats , Collagen , Metabolism , Creatine Kinase , Metabolism , Ischemic Postconditioning , Matrix Metalloproteinase 2 , Metabolism , Myocardial Reperfusion Injury , Myocardium , Metabolism , Rats, Sprague-Dawley , Real-Time Polymerase Chain Reaction , Tissue Inhibitor of Metalloproteinase-2 , Metabolism , Ventricular Function, Left
2.
Chinese Journal of Applied Physiology ; (6): 81-84, 2014.
Article in Chinese | WPRIM | ID: wpr-236379

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of ischemic postconditioning on the expression of rat myocardium matris metalloproteinase-2 (MMP-2) induced by ischemia/reperfusion (I/R) and relationship between its expression and interstitium and the effect on left ventricular function.</p><p><b>METHODS</b>Twenty-four rats were randomly divided into 3 groups (n = 8): sham control (SC) group, ischemic/reperfusion (I/R) group and ischemic postconditioning (IPTC) group. The left ventricular peak systolic pressure and its derivate (+/- dp/dt) were calculated; The amount of myocardium collagenous were determined; The vitality of superoxide dismutase (SOD) and content of malondialdehyde (MDA) of plasma were detected; The activity of myocardium MMP-2 was measured by Western blot and RT-PCR.</p><p><b>RESULTS</b>As compared with I/R group, IPTC could lower the expression of MMP-2, ameliorate left ventricular function and increase the content of myocardium collagenous. In the meantime, the vitality of superoxide dismutase (SOD) of plasma were greatly enhanced and the content of malondialdehyde (MDA) of plasma were reduced in IFC group.</p><p><b>CONCLUSION</b>Protective effect of IPIC on myocardium may be due to reduce free radical, lower expression of MMP-2 and protect myocardial interstitium. MMPs plays an important role in the myocardial protection provided by IPTC.</p>


Subject(s)
Animals , Rats , Collagen , Metabolism , Ischemic Postconditioning , Malondialdehyde , Metabolism , Matrix Metalloproteinase 2 , Metabolism , Myocardial Reperfusion Injury , Myocardium , Metabolism , Rats, Sprague-Dawley , Superoxide Dismutase , Metabolism
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