心血管支架置入与血清补体C3的变化

Serum complement C3 changes following cardiovascular stent implantation

补体系统是由35种广泛存在于血清、组织液和细胞膜表面具有酶活性的蛋白质组成的反应系统,在机体抗感染第一线防御中起重要作用。补体异常活化也参与许多炎症性疾病的发生和发展,补体的激活有3条途径,即经典途径、旁路途径和凝集素途径。心血管支架置入后,冠状动脉粥样硬化性心脏病患者血管内皮有不同程度损伤,血清补体C3可以进入动脉管壁,损伤深层的动脉细胞,使动脉壁的通透性增强,并释放血管壁结构抗原成分,诱导抗体产生,使固定免疫复合物形成,进而诱发血小板在此聚集、黏附或引起该处脂质沉积。尽管心血管支架置入后患者体液免疫亢进,但抵御外来微生物的能力减弱,从而刺激机体产生更多的C3进行自我保护,使炎症进一步加重,循环复合物增多,激活补体系统,进一步导致血管内皮损伤加剧。提示C3在缺血性心血管疾病的发生、发展中起非常重要的作用,是缺血性心血管疾病一个很好的标志物,同时也是心血管支架置入后再狭窄和血栓形成的重要原因之一。

Complement system is a reaction system comprising 35 proteins with enzyme activity common in serum, tissue fluid and cell membrane. It plays an important role in anti-infection. Abnormal complement activation is involved in incidence and progression of many inflammatory diseases. The complement is activated through typical, alternative and agglutinin pathways. Following cardiovascular stent implantation, the vessel endothelium of patients with coronary atherosclerotic heart disease is damaged; serum complement C3 could enter the arterial wall to damage arterial cells to enhance the permeability release antigenic components of vessel wall, and induce antibody production. The fixing immune complex is formed and induces platelet aggregation, attachment or lipidoses. Although humoral immunity becomes accentuated following cardiovascular stent implantation, the capability to resist microorganism is reduced, which stimulates self-protection of C3, aggravates inflammation, increases circulation complex, activates complement system and aggravates endothelial injury. C3 plays an essential role in occurrence and development of ischemic cardiovascular disease, and is an important cause for restenosis and thrombosis following cardiovascular stent implantation.