Abstract
目的：探讨临产前后bcl-2、Fasl在胎盘滋养层细胞的蛋白表达变化及其与母血、羊水中内皮素-1 (Endothelin-1, ET-1)、前列腺素E2 (ProstaglandinE2, PGE2)的浓度之间的关系。方法：53例足月妊娠妇女分成两组，其中临产组28例，未临产组25例。用免疫组化(Immunohistochemical, IHC)法测定胎盘滋养层细胞bcl-2、Fasl的蛋白表达，用放射免疫法测定孕妇母血、羊水中ET-1、PGE2的浓度。结果：1) 临产组胎盘滋养层细胞bcl-2、Fasl的蛋白表达明显低于未临产组，两组平均灰度及阳性细胞率比较，差异有显著性(p 0.05)。结论：bcl-2、Fasl介导的胎盘滋养层细胞凋亡在启动分娩发动过程中具有重要作用；bcl-2的作用可能受ET-1、PGE2等细胞因子的调控。 Objective: To investigate the expressions of bcl-2 and Fasl proteins in placental trophoblastic cells on labor onset and their relationships with the concentrations of Endothelin-1 and Prostaglandin E2 in maternal blood and amniotic fluid. Methods: Fifty-three women on term pregnancy were divided into two groups. One group on the time of labor onset was twenty-eight women. Another group not on the time of labor onset was twenty-five women. Expressions of bcl-2 and Fasl proteins in placental trophoblastic cells were detected by immunohistochemical assay. The concentrations of ET-1 and PGE2 in maternal blood and amnionotic fluid were detected by radioimmune assay. Results: 1) Expressions of bcl-2 and Fasl proteins in the group of labor onset were significantly lower than that in the group of not labor onset. There was a statistically difference in the average gray scale and the ratio of positive cells between the two groups (p < 0.05). 2) The concentrations of ET-1 and PGE2 in maternal blood and amniotic fluid of labor onset group were higher than that of not labor onset group (p < 0.05). 3) There was a positive correlation between the concentrations of ET-1 and PGE2 in maternal blood and amniotic fluid, and the expression of bcl-2 proteins had a negative correlation with the concentrations of ET-1 and PGE2 respectively, but there was no correlation between the expression of Fasl proteins and the concentrations of ET-1 and PGE2. Conclusions: It was considered that the apoptosis of placental trophoblastic cells induced by bcl-2 and Fasl may play an important role in the initiation of term labor onset. ET-1 and PGE2 may control the expression of bcl-2.
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