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生物学途径协同作用与胎膜早破的研究进展
引用本文:刘文翠,白玉芳,穆婉茹,路丽,祁存秀,苏占海,王荣华.生物学途径协同作用与胎膜早破的研究进展[J].国际妇产科学杂志,2018,45(5):544-548.
作者姓名:刘文翠  白玉芳  穆婉茹  路丽  祁存秀  苏占海  王荣华
作者单位:810001西宁,青海大学附属医院
基金项目:青海省应用基础研究项目(2016-ZJ-762)
摘    要:胎膜早破(PROM)是围生期胎儿发病率和死亡率增加的一个危险因素。现有资料及医学技术仍难以精准预测胎膜早破的发生,了解PROM的发生机制,准确及时诊断PROM对减少母婴感染至关重要。研究发现,细胞因子、凝血酶和基质金属蛋白酶激活、氧化应激和凋亡是PROM发生的主要生物学途径。而这些生物过程是由包括感染、炎症、胎盘出血和子宫过度膨胀在内的多种病因引起的,将各个生物学途径的协同作用与胎膜的弱化联系起来探讨PROM的生物学发生机制,从生物学角度对胎膜早破的预测和防治找到突破口,对现代医学意义重大。

关 键 词:胎膜早破  细胞因子类  基质金属蛋白酶类  凝血酶  细胞凋亡  氧化性应激  
收稿时间:2018-05-18

Research Progress of Biological Pathway Synergistic Effect and Premature Rupture of Membranes
LIU Wen-cui,BAI Yu-fang,MU Wan-ru,LU Li,QI Cun-xiu,SU Zhan-hai,WANG Rong-hua.Research Progress of Biological Pathway Synergistic Effect and Premature Rupture of Membranes[J].Journal of International Obstetrics and Gynecology,2018,45(5):544-548.
Authors:LIU Wen-cui  BAI Yu-fang  MU Wan-ru  LU Li  QI Cun-xiu  SU Zhan-hai  WANG Rong-hua
Affiliation:The Affiliated Hospital of Qinghai University,Xining 810001,China
Abstract:Premature rupture of membranes(PROM) is a risk factor for increased fetal morbidity and mortality during perinatal period. Existing data and medical techniques are still difficult to accurately predict the occurrence of premature rupture of membranes, it is essential to understand the mechanism of PROM and accurately diagnose PROM to reduce maternal and child infections. Existing studies have found that cytokines, thrombin and matrix metalloproteinase activation, oxidative stress and apoptosis are the main biological pathways of PROM. These biological processes are caused by a variety of causes including infection, inflammation, placental hemorrhage and excessive uterine uterus. To explore the biological mechanism of PROM by combining the synergistic actions of various biological pathways with the weakening of the membrane and to find a breakthrough in the prediction and prevention of PROM is of great significance to modern medicine.
Keywords:Fetal membranes  premature rupture  Cytokines  Matrix metalloproteinases  Thrombin  Apoptosis  Oxidative stress  
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