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目的:探讨母胎界面上Fas及其配体FasL表达与妊娠期高血压疾病的关系。方法:采用免疫组化方法对49例产妇母胎界面上Fas及其配体FasL表达进行测定,其中正常孕足月产妇16人,妊娠期高血压疾病轻度子痫前期产妇18名,妊娠期高血压疾病重度子痫前期15名,所有患者均为剖宫产分娩。结果:妊娠期高血压疾病组胎盘滋养细胞Fas表达较正常孕足月组增强并随病情加重更为明显,而FasL着色较正常孕足月组减弱,随病情加重更为明显。在底蜕膜细胞中,随妊娠期高血压疾病的加重FasL表达与正常孕足月相比逐渐减弱。结论:母胎界面Fas及其配体FasL表达紊乱,致使局部免疫反应增强,免役豁免机制被破坏,而高表达的Fas引起胎盘滋养细胞及底蜕膜细胞随之增加,导致胎盘侵蚀异常,血管重铸障碍,可能是妊娠期高血压疾病发病的重要机制之一。
Objective: To investigate the relationship between the expression of Fas and its ligand FasL in maternal-fetal interface and gestational hypertension. Methods: Immunohistochemistry was used to detect the expression of Fas and FasL on the maternal-fetal interface in 49 maternal and fetal fetuses. Among them, 16 were pregnant with normal pregnancy, 18 were mild preeclampsia with gestational hypertension, and were highly gestational Severe preeclampsia hypertension 15 cases, all patients were cesarean section delivery. Results: The expression of Fas in placental trophoblastic cells in gestational hypertension group was significantly higher than that in normal pregnancy group and was more pronounced with the aggravation of symptoms. FasL staining was weaker than that in normal pregnancy group and more severe with aggravation of disease. Decidual cells in the bottom, with the increase of hypertensive disorders during pregnancy, FasL expression and normal pregnancy months gradually weakened. Conclusion: The expression of Fas and FasL in maternal-fetal interface is disturbed, which leads to the increase of local immune response and the destruction of immune-exemption mechanism. However, the high expression of Fas causes the increase of placental trophoblasts and basal decidual cells, resulting in abnormal placenta ablation, Casting obstacles, may be one of the important pathogenesis of hypertensive disorders during pregnancy.