小鼠心肌梗死后补体系统激活与炎症反应的相关性研究

目的:探讨心肌梗死后补体系统激活的作用。方法:采用结扎冠状动脉左前降支的方法,复制心肌梗死小鼠模型,分为心肌梗死组(MI,n=25)与假手术组(Sham,n=12),术后7d超声心动图检测心功能;心肌组织HE染色观察炎症细胞浸润、Masson染色和天狼猩红染色观察胶原沉积与纤维化程度;Real-time PCR定量检测心肌组织中C3a与C5a的mRNA表达水平,并对C3a、C5a mRNA表达量与射血分数(EF)之间作相关性分析。结果:术后7d,MI组小鼠的生存率为68.0%,明显低于Sham组(P0.05);MI组的LVAWs、EF、FS均明显降低(P0.05);HE染色可见MI组有大量炎性细胞浸润,Masson染色与天狼猩红染色发现胶原纤维沉积、纤维化面积增加(P0.01);C3a与C5a的mRNA表达量增加,且这两项指标均与EF之间呈负相关。结论:心肌梗死后补体系统被激活,补体系统的活化程度与射血分数的降低有关,提示补体系统可能通过调控心肌组织的炎症反应和纤维化过程,成为加重心脏病理损伤的重要因素。

Activation of the complement system was related with the inflammatory response after myocardial infarction in mice

Objective：To investigate the role of activated complement system after myocardial infarction in mice.Methods：The model of myocardial infarction was copied by ligation the left anterior descending coronary artery.The mice were divided into the MI group （MI,n =25） and the Sham group （Sham,n =12）.The heart function was detected in 7d post-operation by echocardiography.HE staining,Masson staining and Sirius red staining were used to analyze inflammatory cell infiltration,collagen deposition,fibrosis in myocardial tissue.The mRNA levels of C3a and C5a were measured by Real-time PCR.The correlation analysis was used between C3a,C5a mRNA expression and ejection fraction （EF）.Results：The survival rate was 68.0％ in MI mice 7d post-operation,which was significantly lower than that in Sham group （P ＜ 0.05） ; The LVAWs,EF and FS in MI group were decreased （P ＜ 0.05） ; In MI group,there were a large number of inflammatory cells infiltration,deposition of collagen and the fibrosis area increased （P ＜ 0.01）.The level of C3a and C5a mRNA markedly increased and were negatively correlated with EF.Conclusion：The complement system is activated after myocardial infarction.The degree of complement system activation is related with reduced ejection fraction,suggesting that the complement system could regulate the process of inflammation and fibrosis in myocardial tissue.Therefore,the activation of complement system maybe an important factor in aggravated cardiac injury after MI.