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目的研究缺血后处理对体外循环术(CPB)后心肌细胞凋亡的影响,探讨再灌注损伤补救激酶(RISK)信号传导系统中Akt,Erk在心肌细胞凋亡过程调控机制中的作用,研究Bax/Bcl-2基因蛋白表达的差异。方法将10只健康成年杂种犬随机分为对照组和缺血后处理(IPostC)组。分别在开始体外循环之前,阻断循环过程中及开放循环再灌注90min时获取心肌标本,采用免疫组织化学法检测犬心肌细胞中Akt、Erk、Bcl-2及Bax蛋白的表达。采用TUNEL法检测凋亡心肌细胞,计算凋亡指数。结果开放循环再灌注90min后与对照组相比缺血后处理组犬心肌细胞内P-Akt增加(30.7±6.2vs.20.5±3.0,P<0.05),P-Erk(27.6±6.1vs.19.3±3.8,P<0.05),Bcl-2(23.4±6.2vs.14.0±4.3,P<0.05)蛋白表达升高,而Bax(15.8±4.9vs.29.9±7.5,P<0.05)下降。心肌细胞凋亡指数降低(P<0.05)。结论缺血后处理为一种内源性心肌保护性措施和因素,其心肌保护作用机制可能与信号保护通路有关。心肌细胞凋亡是CPB中心肌I/R损伤的重要病理特征之一,IPostC可抑制CPB中缺血再灌注性心肌细胞凋亡的发生。其作用与上调RISK系统及调控Bcl-2/Bax基因有关。
Objective To investigate the effect of ischemic postconditioning on cardiomyocyte apoptosis after cardiopulmonary bypass (CPB), and to explore the role of Akt and Erk in the regulation of cardiomyocyte apoptosis in reperfusion injury repair kinase (RISK) signal transduction system. Difference of Bax / Bcl-2 gene protein expression. Methods Ten healthy adult mongrel dogs were randomly divided into control group and IPostC group. Myocardial samples were obtained before cardiopulmonary bypass (CPB), blocked during circulation and 90 min after reperfusion. The expressions of Akt, Erk, Bcl-2 and Bax protein in canine cardiomyocytes were detected by immunohistochemistry. Apoptotic cardiomyocytes were detected by TUNEL method and apoptotic indices were calculated. Results Compared with the control group, the P-Akt in ischemic postconditioning group (30.7 ± 6.2 vs.20.5 ± 3.0, P <0.05) and P-Erk (27.6 ± 6.1 vs.19.3 ± 3.8, P <0.05). The protein expression of Bcl-2 (23.4 ± 6.2 vs 14.0 ± 4.3, P <0.05) increased while Bax decreased (15.8 ± 4.9 vs 29.9 ± 7.5, P <0.05). Myocardial apoptosis index decreased (P <0.05). Conclusion Ischemic postconditioning is a kind of endogenous myocardial protective measures and factors, and its myocardial protective mechanism may be related to signal protection pathway. Cardiomyocyte apoptosis is one of the important pathological features of I / R injury in CPB myocardium. IPostC can inhibit the apoptosis of ischemia-reperfusion cardiomyocytes in CPB. Its role and up RISK system and regulation of Bcl-2 / Bax gene.