缺氧诱导滋养细胞自噬参与子痫前期发病的实验研究  

Experimental study of hypoxia-inducible trophoblastic autophagy involved in the pathogenesis of preeclampsia

作　　者：秦兴发[1] 张华[1] 漆洪波[1] 陈国庆[2] 马海霞[1] 

机构地区：[1]重庆医科大学附属第一医院产科,400016 [2]广东省深圳市妇幼保健院妇产科,518000

出　　处：《重庆医学》2014年第5期569-571,共3页Chongqing medicine

基　　金：国家自然科学基金资助项目(81070502);国家临床重点专科建设项目经费资助

摘　　要：目的探讨缺氧环境下滋养细胞自噬及子痫前期患者胎盘组织自噬发生情况。方法将滋养细胞株HTR-8/SVneo分为低氧浓度Ⅰ、Ⅱ组及正常氧浓度组,处理48h后应用激光共聚焦显微镜检测细胞质内自噬体,PCR分析自噬相关基因LC3-Ⅱ的表达变化;免疫组织化学检测30例子痫前期患者胎盘组织LC3-Ⅱ表达水平。结果低氧浓度组细胞质内可见红色自噬体染色结构,而正常氧浓度Ⅰ、Ⅱ组则极少见,低氧浓度Ⅰ、Ⅱ组细胞LC3-ⅡmRNA表达量明显高于正常浓度组(P<0.05),子痫前期患者胎盘组织LC3-Ⅱ免疫染色阳性率为67.12%,而正常浓度组则为9.14%,两组间差异具有统计学意义(P<0.05)。结论子痫前期患者胎盘组织细胞自噬活性增高,缺氧可诱导滋养细胞株发生自噬现象。Objective To study hypoxia environment trophoblast cell autophagy and autophagy of the preeclampsia placental tis-sue .Methods Trophoblastic cell line HTR-8/SVneo were divided into three groups ：low oxygen concentration group （group Ⅰand group Ⅱ） and normal oxygen concentration group ;48 h after the application the confocal laser scanning microscopy was used for detection of cytoplasmic autophagosome ,PCR technology analysis of autophagy-related gene expression change of LC3-Ⅱ .LC3-Ⅱ expression levels of 30 cases of preeclampsia placenta were detected by Immunohistochemistry .Results In low oxygen concen-tration group ,there were visible red autophagosome chromatin structure in cytoplasm ,which was extremely rare in the normal oxy-gen concentration group ,in low oxygen concentration group cell LC3-Ⅱ mRNA expression was significantly higher than that of normal concentration group .The preeclampsia placenta of patients with positive immunostaining of LC 3-Ⅱ was 67 .12% ,compared with 9 .14% in the normal control ,there was a significant difference between two groups .Conclusion Preeclampsia placenta auto-phagy activity increased ,hypoxia can induce autophagy trophoblast cell line phenomenon .

关 键 词：自噬 缺氧 子痫前期 

分 类 号：R714.245[医药卫生—妇产科学]