早产炎性病因的研究进展

摘要/Abstract

摘要： 早产（preterm birth，PTB）是常见的产科并发症，对母胎危害极大。目前PTB分娩发动的机制尚不清楚。现有研究表明，炎症反应在PTB的发动中发挥重要的作用，尤其是炎症介质，一方面促进前列腺素合成释放，诱发宫缩；另一方面促进宫颈成熟，激活基质金属蛋白酶降解细胞外基质，降低胎膜韧度。以上综合作用最终引起子宫收缩、宫颈成熟、胎膜破裂，导致PTB。微生物感染和机体的氧化应激、自噬抑制等均可引起炎症反应。大气污染中细颗粒物（PM2.5）可能通过诱发宫内轻度炎症，造成PTB发生。PTB机制尚不明确，现从炎症介导PTB的相关分子、引起炎症的生物和非生物学途径等几个方面综述PTB的发生。

关键词: 早产, 胎膜早破, 感染, 细胞因子类, 非生物学因素

Abstract: Preterm birth (PTB) is a common obstetric complications and it is greatly harmful to mothers and fetals. At present, the mechanism of PTB is not clear. The present research shows that the inflammatory response, especially the inflammatory mediators，plays an important role in the initiation of PTB. The inflammatory mediators on one hand promote the synthesis of prostaglandin and induce uterine contractions, on the other hand promote cervical ripening and trigger matrix metalloproteinases to degrade extracellular matrix, reduce toughness of fetal membranes. The combined effect of all above finally cause uterine contraction, cervical ripening, rupture of fetal membranes, leading to PTB. Microbial infection and the oxidative stress, inhibited autophagy can cause inflammation. PM2.5 may induce mild intrauterine inflammation, resulting in PTB. Mechanism of PTB is unknown and this article will review the mechanism from three aspects. They are the related molecules in inflammation-mediated PTB, the biological and non-biological pathways inducing inflammation.

Key words: Premature birth, Fetal membranes, premature rupture, Infection, Cytokines, Nonbiological factor

耿倩，常颖，陈叙. 早产炎性病因的研究进展[J]. 国际妇产科学杂志, 2018, 45(1): 19-22.

GENG Qian，CHANG Ying，CHEN Xu. Advances in Inflammatory Causes of Preterm Birth[J]. Journal of International Obstetrics and Gynecology, 2018, 45(1): 19-22.

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