PI3K/AKT通路在稽留流产发病中的作用研究  

The role of PI3K/AKT pathway in the pathogenesis of missed abortion

作　　者：夏妍芬 植枝福[1] 梁爽[1] 吴巧灵 Xia Yanfen;Zhi Zhifu;Liang Shuang;Wu Qiaoling(Department of Obstetrics and Gynecology,the First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China)

机构地区：[1]广西医科大学第一附属医院妇产科,南宁530021

出　　处：《广西医科大学学报》2020年第11期2003-2008,共6页Journal of Guangxi Medical University

摘　　要：目的:探讨PI3K/AKT信号通路在稽留流产发病过程中的相关作用机制。方法:选取在广西医科大学第一附属医院诊断为稽留流产行人流术的患者与正常早孕要求行人流术者各30例作为研究对象,取两组绒毛组织应用免疫组化检测PI3K、AKT的表达量并对比其差异,初步判断PI3K、AKT与稽留流产之间的关系。取HTR8/SVneo细胞培养,分为3组:常氧组、低氧组及低氧下加LY294002组,其对应的处理方式分别为:常氧培养、单纯低氧刺激及单纯低氧刺激加PI3K抑制剂LY294002,应用Western blotting检测各组细胞AKT、VEGF表达量的变化,应用成管实验检测各组细胞的成管能力变化。结果:稽留流产组绒毛组织的PI3K、AKT平均光密度比早孕人流组更低(均P<0.05)。低氧组AKT、VEGF的表达水平高于常氧组(P<0.05),但低氧下加LY294002组的AKT、VEGF的表达水平低于低氧组(P<0.05);低氧组的管腔形成能力高于常氧组(P<0.05),同样低氧下加LY294002组的管腔形成能力亦低于低氧组(P<0.05)。结论:在低氧环境中抑制PI3K/AKT信号通路可下调VEGF表达水平并下调滋养细胞的管腔形成能力,推断PI3K/AKT的表达水平降低与稽留流产发病相关。Objective:To investigate the mechanism of PI3K/AKT signaling pathway in the pathogenesis of missed abortion.Methods:Thirty patients with missed abortion diagnosed in our hospital and 30 patients with normal early pregnancy requiring abortion were selected,and the villi tissues were taking to detect PI3K and AKT expressions by immunohistochemical technology.The relationship between PI3K/AKT and missed abortion was preliminarily analyzed.HTR8/SVneo cells were cultured and divided into three groups:normoxia group,hypoxia group and hypoxia+LY294002 group.Western blot was used to detect the expression levels of AKT and VEGF in HTR8/SVneo cells after different treatments,and the tubular formation experiment was used to detect the tubular formation capacity of HTR8/SVneo cells.Results:The average optical density of PI3K and AKT in the missed abortion group was lower than that in early pregnancy requiring abortion group(P<0.05).The expression level of AKT and VEGF in the hypoxia group was higher than that in the normoxia group(P<0.05),but the expression level of AKT and VEGF in the hypoxia+LY294002 group was lower than that in the hypoxia group(P<0.05).The lumen forming ability of the hypoxia group was higher than that of the normoxia group(P<0.05),and the lumen forming ability of the hypoxia+LY294002 group was also lower than that of the hypoxia group(P<0.05).Conclusion:The expressions of PI3K and AKT are decreased in the villi of patients with missed abortion,while the inhibition of PI3K/AKT signaling pathway in the hypoxic environment can down-regulate the expression level of VEGF and reduce the lumen formation capacity of trophoblast cells,thus it can be inferred that the decreased expression level of PI3K/AKT is related to the incidence of missed abortion.

关 键 词：PI3K/AKT 稽留流产 低氧 滋养细胞 血管形成 

分 类 号：R714.21[医药卫生—妇产科学]