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目的探讨人胎盘滋养细胞过度自噬参与早发型子痫前期的病理及分子机制。方法 (1)收集重庆医科大学附属第一医院2010年1月至2012年5月分娩的18例早发型子痫前期和20例正常产妇的胎盘组织。应用免疫组化检测胎盘组织中自噬相关蛋白LC3和Beclin-1的表达及定位。(2)以葡萄糖氧化酶模拟氧化应激环境,通过Western-blot方法测定处理后的人绒毛外滋养细胞株HTR8/SVneo自噬发生的情况,Transwell侵袭实验检测细胞侵袭能力。结果 (1)免疫组化提示早发型子痫前期胎盘滋养细胞LC3和Beclin-1表达量较正常胎盘增高(P<0.05)。(2)Western-blot均提示氧化应激条件下HTR8/SVneo自噬发生增加,Transwell侵袭实验提示经处理后的滋养细胞侵袭力降低。结论滋养细胞发生过度自噬可能是早发型子痫前期胎盘功能紊乱的另一重要发病机制。
Objective To investigate the pathological and molecular mechanisms of human placental trophoblast cells participating in autophagy over pre-eclampsia. Methods (1) The placenta tissues of 18 preeclampsia and 20 normal pregnant women who were delivered from January 2010 to May 2012 in the First Affiliated Hospital of Chongqing Medical University were collected. The expression and localization of autophagy-related proteins LC3 and Beclin-1 in placenta were detected by immunohistochemistry. (2) The oxidative stress environment was simulated by glucose oxidase. The autophagy of human chorionic villus cell line HTR8 / SVneo was detected by Western-blot. Transwell invasion assay was used to detect cell invasion. Results (1) Immunohistochemistry showed that the expression of LC3 and Beclin-1 in placental trophoblast cells in early onset preeclampsia was higher than that in normal placenta (P <0.05). (2) Both Western-blot showed that autophagy was increased in HTR8 / SVneo cells under oxidative stress. Transwell invasion assay suggested that the invasiveness of the treated cells decreased. Conclusion Trophoblast over-autophagy may be another important pathogenesis of placental dysfunction in early-onset preeclampsia.