先兆子痫患者母胎界面上细胞凋亡的研究

目的:研究先兆子痫患者母胎界面上细胞凋亡水平及凋亡相关分子的表达变化。方法:分别收集妊娠25、27、29、30和31周及足月分娩的正常妊娠者和先兆子痫患者的胎盘组织,采用脱氧核糖核酸末端转移酶介导的dUTP刻痕末端标记法(TUNEL)检测母胎界面上细胞凋亡情况, 并行凋亡细胞定位;RT-PCR检测正常妊娠和先兆子痫胎盘组织中P53,Bcl-2和Bax的mRNA表达水平的差异。结果:正常妊娠和先兆子痫患者胎盘中发生凋亡的细胞数目都随孕周延长而逐渐增高,但先兆子痫的胎盘中细胞凋亡率明显高于正常妊娠者;正常妊娠胎盘中凋亡细胞主要为合体滋养层细胞,足月胎盘绒毛内血管内皮细胞亦有少量细胞凋亡,而先兆子痫胎盘中细胞滋养层细胞、合体滋养层细胞和绒毛内血管内皮细胞均发生明显的凋亡;RT-PCR显示先兆子痫胎盘组织中P53和Bax的mRNA水平明显高于同期妊娠的正常胎盘,而Bcl-2水平显著降低。结论:正常妊娠过程中胎盘组织中只在有限部位出现少量细胞凋亡,而先兆子痫胎盘组织中细胞过度凋亡, 且凋亡细胞分布广泛,并伴有凋亡相关分子的表达上调。表明先兆子痫的发生与胎盘组织中滋养层细胞大量凋亡密切相关。

Study on Cell Apoptosis in the Placenta of Preeclampsia

Objective: To study the difference of cell apoptosis and the expression of apoptosis-related molecules (P53, Bcl-2 and Bax) in the placentas of normal pregnancy and preeclampsia. Methods: Placentas were collected from women with normal pregnancy or preeclampsia when they gave birth at gestational weeks 25, 27, 29, 30, 31 and term. Cell apoptosis was detected by TUNEL, and the mRNA expression of P53, Bcl-2 and Bax was examined by semi-quantitative RT-PCR. Results: Cell apoptosis occurred in placentas of both normal pregnancy and preeclampsia. The number of apoptotic cells in placentas of normal pregnancy increased with the advance of gestational stages, however, there were much more apoptotic cells in placenta of preeclampsia compared with that of normal pregnancy. Obvious apoptosis was observed in cytotrophoblasts, syncytiotrophoblasts and villous endot-helial cells in the placenta of preeclampsia, while only small amount of syncytiotrophoblasts and endothelial cells showed apoptosis in normal placenta. The mRNA expression level of P53 and Bax increased and Bcl-2 decreased in placenta of preeclampsia compared with that of normal pregnancy. Conclusion: Cell over apoptosis occurred extensively in placentas of preeclampsia, with up-regulated expression level of apoptosis-related molecules whereas a small amount of apoptosis cells occurred in placentas with limited lacations of normal pregnancy. The data suggested that the pathogenesis of preeclampsia is greatly correlated with over-apoptosis of trophoblastic cells.