补体1抑制剂抑制缺血心肌细胞凋亡及其机制  

Anti-Apoptotic Activity of C1 Inhibitor in Ischemic Reperfused Myocardium and Its Mechanisms

作　　者：付金容[1] 黎明江[1] 周艳丽[1] 林国生[1] 

机构地区：[1]武汉大学人民医院心内三科,湖北武汉430060

出　　处：《武汉大学学报（医学版）》2014年第5期670-673,共4页Medical Journal of Wuhan University

摘　　要：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 explore the anti-apoptotic activity and its mechanisms of C1inhibitor（C1INH）in ischemic reperfused myocardium.Methods：Models of rat heart ischemia/reperfusion（I/R）were established,and the effect of C1 INH intervention was observed on myocardium through detecting the apoptosis of cardiocytes by TUNEL（ischemia/reperfusion）and assaying the expression of Bcl-2,Bax,caspase-3,and cleaved caspase-3by Western blot.We also assayed the activity of caspase-3in serum.Results：C1INH intervention significantly reduced the apoptosis of cardiocytes（P〈0.05）.The proportion of Bcl-2/Bax expression was reversed,and the expression levels of caspase-3and cleaved caspase-3in myocardium and the caspase-3activities in serum were reduced.Conclusion：C1INH,in addition to the inhibition on the activation of complement and inflammation,improves the outcome of I/R-mediated myocardial cell injury via the anti-apoptotic activity.

关 键 词：补体1抑制剂 凋亡 缺血再灌注 Bcl-2 BAX CASPASE-3 

分 类 号：R332[医药卫生—人体生理学]