| AimsObserve the effect of ischemia-reperfusion injury on Pim-3 gene expression in myocardial tissue and explore the possible molecular mechanism.MethodsPim-3 gene expression in intact rat heart tissue was detected using RT-PCR ,western blot and immunohistochemical assay. The model of myocardial Ischemia-reperfusion injury was established. 30 SD male adult rats were randomly divided into 5 groups. The left anterior descending coronary artery were ligated for about 15min, 30min, or ligated for 30min before reperfusion for another 30min, or 120min. Left ventricular tissues were removed immediately. Pim-3 gene expression was analyzed using RT-PCR method and immunohistochemical assay. Neonatal cardiomyocytes were dealed with different concentrations of H2O2 (0μM, 5μM, 10μM, 20μM) and tumor necrosis factor-α(TNF-α, 0ng/ml, 1ng/ml, 5ng/ml, 10ng/ml). Pim-3 gene expression was detected by RT-PCR method. Cardiomyocytes were transfected with Pim-3 siRNA fragment and induced apoptosis with H2O2.ResultsThe results showed that normal myocardial tissue express Pim-3 gene mRNA and protein. Ischemia and reperfusion injury induced Pim-3 gene expression in myocardial tissue. Furthermore, H2O2 but not TNF-αincreased Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing did not facilitated H2O2 induced apoptosis in cardiomyocytes.ConclusionIt was concluded that ischemia-reperfusion injury induced Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissue.
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