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复发性流产(recurrent spontaneous abortion,RSA)为与同一性伴侣发生连续3次或3次以上的自然流产。补体激活的适当抑制是正常妊娠所必需的,母胎界面补体过度激活可导致胚胎死亡、RSA等妊娠并发症。流产动物模型表明补体系统由经典途径或旁路途径激活,产生的C3a、C5a趋化激活中性粒细胞或单核细胞,促使其分泌B因子、D因子,激活、放大旁路途径,形成补体激活的恶性循环。活化的中性粒细胞或单核细胞经可溶性血管内皮生长因子受体1(sFlt-1)途径和组织因子(TF)途径导致RSA等妊娠并发症。但目前对于补体异常激活的关键途径、重要补体组分及致RSA的机制尚不清楚,有待于进一步的研究。
Recurrent spontaneous abortion (RSA) is spontaneous abortion that occurs 3 or more times in a row with the same-sex partner. Appropriate inhibition of complement activation is necessary for normal pregnancy, maternal-fetal interface over-activation of complement can lead to embryo death, RSA and other pregnancy complications. Animal models of abortion indicate that the complement system is activated by the classical or alternative pathways and that C3a and C5a chemotactic activates neutrophils or monocytes that cause them to secrete factor B and factor D to activate and amplify the alternative pathway to form complement Activation of the vicious circle. Activated neutrophils or monocytes lead to pregnancy complications such as RSA via the soluble vascular endothelial growth factor receptor 1 (sFlt-1) pathway and the tissue factor (TF) pathway. However, at present, the key pathway of abnormal activation of complement, the important complement component and the mechanism of RSA are not clear yet, which needs further study.