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目的:探讨补体1抑制剂(C1INH)对缺血再灌心肌细胞凋亡的影响及作用机制。方法:复制大鼠缺血再灌注模型,C1INH进行干预,实验分为假手术组、NaCl组及C1INH组。TUNEL法检测心肌组织的心肌细胞凋亡情况。Western blot检测心肌组织Bcl-2、Bax、Caspase-3及Cleaved caspase-3的表达情况。同时测定血浆Caspase-3的活性。结果:与对照组比较,C1INH干预组心肌细胞的凋亡明显减少(P<0.05)。同时C1INH干预组Bcl-2和Bax的表达比例更趋于正常化,Caspase-3及Cleaved caspase-3的表达及活性则明显减少(P<0.05)。结论:在心肌的缺血再灌中,C1INH,除了抑制补体激活,抑制炎症反应而对心肌细胞具有保护作用外,还能通过通过平衡Bcl-2和Bax的表达,抑制Caspase-3的活性及裂解而对抗心肌细胞的凋亡。
Objective: To investigate the effects of complement inhibitor 1 (C1INH) on myocardial cell apoptosis after ischemia-reperfusion and its mechanism. Methods: The rat model of ischemia-reperfusion was established, C1INH was used for intervention. The experiment was divided into sham operation group, NaCl group and C1INH group. TUNEL method was used to detect myocardial cell apoptosis in myocardium. Western blot was used to detect the expression of Bcl-2, Bax, Caspase-3 and Cleaved caspase-3 in myocardium. Simultaneous determination of plasma Caspase-3 activity. Results: Compared with the control group, the apoptosis of cardiomyocytes in C1INH group was significantly decreased (P <0.05). At the same time, the expression of Bcl-2 and Bax in C1INH intervention group tended to be normalized. The expression and activity of Caspase-3 and Cleaved caspase-3 were significantly decreased (P <0.05). CONCLUSION: In myocardial ischemia-reperfusion, C1INH inhibits the activation of complement and inhibits the inflammatory response and protects cardiomyocytes. It can also inhibit the activity of Caspase-3 by balancing the expressions of Bcl-2 and Bax and Lysis against cardiomyocyte apoptosis.