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机构地区:[1]武汉大学人民医院心内三科,武汉湖北430060
出 处:《海南医学》2013年第1期6-8,共3页Hainan Medical Journal
摘 要:目的研究缺血再灌注心肌中补体C3的表达以及补体1抑制剂(C1INH,C1inhibitor)对缺血心肌的保护作用。方法结扎大鼠的冠状动脉左前降支30min,再灌注3h、72h造成缺血再灌损伤模型。实验分为假手术组、NaCl组和C1INH组(每组5只大鼠,n=5),观察C1INH对大鼠心功能、心肌梗死面积的影响,同时采用免疫组化和Western blot法检测缺血心肌补体C3的表达。结果与假手术组比较,再灌注3h及72h后,NaCl组和C1INH组鼠心功能下降,心肌的梗死面积增加,缺血心肌补体C3的表达增加。与NaCl组比较,再灌注72h后,C1INH组心功能改善,心肌的梗死面积减少[(36.28±0.99)%vs(50.58±0.24)%],差异具有统计学意义(P<0.05)。同时,C1INH组缺血心肌补体C3的表达减少。结论 C1INH通过抑制缺血心肌补体C3的表达而减少缺血再灌所致的心肌损伤,改善心功能。Objective To explore the expression of C3 in ischemic reperfused myocardium and the protec- tive effect of C 1 inhibitor (C11NH) on ischemic myocardium. Methods Rat heart ischemia/reperfusion injury was induced by occluding the left anterior descending coronary artery for 30 min and reperfusion for 3 h or 72 h. C1 inhibitor or NaC1 was administrated intravenously 5 min before surgery. The rats were divided into three groups, the false surgery group, the NaC1 group and the CIINH group, each with 5 cases. The effect of CIlNH on cardiac function and infarct size was measured, and the expression of C3 in ischemic myocardium was detected by immunohistochemistry and western blot. Results 3 h and 72 h after reperfusion, the NaC1 group and the C 11NH group had worsened cardiac function and increased infarct size, as well as increased expression of C3, compared with the false surgery group. 72 h after reperfusion, the CIINH group had significantly improved cardiac function and significantly reduced infarct size [(36.28±0.99)% vs (50.58±0.24)%], compared with the NaCI group (P〈0.05), as well as suppressed expression of C3. Conclusion CIINH protects against I/R-induced myocardial injury via inhibition of C3 protein expression in isch- emic myocardium.
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