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目的探讨先兆子痫患者胎盘组织中尿皮素(UCN)和促肾上腺皮质激素释放激素2β受体(CRH R2β)表达与先兆子痫发病的关系。方法应用半定量RT PCR技术测定20例先兆子痫患者(先兆子痫组)和20例正常妊娠妇女(对照组)胎盘组织中UCNmRNA和CRH R2βmRNA的水平;采用免疫组化方法对UCN进行蛋白定位和半定量分析。结果(1)先兆子痫组胎盘组织中UCNmRNA的表达水平为1 14±0 26,高于对照组的0 78±0 46,两组比较,差异有统计学意义(P<0 05)。(2)先兆子痫组胎盘组织中CRH R2βmRNA的表达水平为0 89±0 33,与对照组的0 93±0 50比较,差异无统计学意义(P>0 05)。(3)免疫组化定位结果显示,两组产妇的UCN蛋白表达主要位于合体滋养细胞,少量表达于细胞滋养细胞和血管内皮细胞。蛋白半定量结果显示,UCN在先兆子痫组胎盘合体滋养细胞中的表达强度高于对照组,两组比较,差异有统计学意义(P<0 05 )。结论先兆子痫患者胎盘组织中UCN表达水平升高,而CRH R2β水平则无明显变化,因此UCN的作用加强。这可能是胎盘组织对母体和胎儿应激状态的一种继发性代偿反应,并参与先兆子痫的病理生理过程。
Objective To investigate the relationship between the expression of UCN and CRH R2β in the placenta of preeclampsia and the pathogenesis of preeclampsia. Methods The levels of UCN mRNA and CRH R2β mRNA in placentas from 20 preeclampsia patients (preeclampsia group) and 20 normal pregnant women (control group) were determined by semi-quantitative RT-PCR. The protein localization of UCN was determined by immunohistochemistry And semi-quantitative analysis. Results (1) The expression of UCN mRNA in placental tissue of preeclampsia group was 114 ± 0 26, which was higher than that of the control group (0 78 ± 0 46). There was significant difference between the two groups (P <0.05). (2) The expression level of CRH R2β mRNA in placental tissue of preeclampsia group was 0 89 ± 0 33, which was not significantly different from 0 93 ± 0 50 in control group (P> 0.05). (3) Immunohistochemical localization results showed that UCN protein expression in the two groups was mainly located in syncytiotrophoblast cells, a small amount expressed in cytotrophoblasts and vascular endothelial cells. Protein semiquantitative results showed that the expression of UCN in pre-eclampsia group was significantly higher than that of the control group. There was significant difference between the two groups (P <0.05). Conclusions The level of UCN in placenta of preeclampsia patients is elevated, while the level of CRH R2β is unchanged. Therefore, the effect of UCN is enhanced. This may be a secondary compensatory response of placental tissue to maternal and fetal stress and participate in the pathophysiological process of preeclampsia.