基质金属蛋白酶降解胞外基质致未足月胎膜早破研究进展  

Research Progress of Matrix Metalloproteinases in Preterm Premature Rupture of Membranes through Degrading Extracellular Matrix

作　　者：李雯[1] 常颖[1] 李星[2] 徐亚玲[2] 陈叙[1] 

机构地区：[1]天津市中心妇产科医院,300100 [2]天津医科大学

出　　处：《国际妇产科学杂志》2016年第1期8-10,共3页Journal of International Obstetrics and Gynecology

摘　　要：早产是威胁围生儿生命健康的首要病因。据统计,2012年中国早产发生率为8.1%。未足月胎膜早破（preterm premature rupture of membranes,PPROM）占早产的25%~30%,重要诱因为宫内感染。近年研究发现,PPROM的分子机制为胎膜组织中胞外基质过早降解,主要由基质金属蛋白酶（matrix metalloproteinases,MMPs）在胎膜组织中的激活引起。MMPs的激活原因有炎症因子的表达增高,如白细胞介素1（IL-1）,IL-6以及肿瘤坏死因子α（TNF-α）,但具体机制尚有待研究。MMPs在正常分娩与PPROM发生过程中的激活、分泌及其影响因素仍需探索,其可能作为预测妊娠结局的标记物,为PPROM的预防与治疗提供突破点。Preterm birth is the first critical factor of life, threatening diseases for the perinatal. According to the statistics,the preterm birth rate in China reached 8.1% in 2012. And the frequency of preterm premature rupture of membranes（PPROM）is about 25%-30%, and intrauterine infection is the principal element. The recent research shows that a molecular mechanism of PPROM is advanced degradation of extracellular matrix, which due to the activation of matrix metalloproteinases（MMPs） in fetal membrane. The high expression of cytokines, such as IL-1, IL-6 and TNF-α, maybe the reason of MMPs′ activation. The process of activation and secretion of MMPs in term labor and preterm birth still need to be explored, which may be considered as a marker of pregnancy outcome. MMPs can provide a breakpoint of prevention and therapy for PPROM.

关 键 词：基质金属蛋白酶类 感染 细胞因子类 早产 胎膜早破 

分 类 号：R714.433[医药卫生—妇产科学]