关于妊娠期肝内胆汁淤积症胎盘细胞凋亡与围生儿缺氧关系的研究

　　【摘要】 目的：探讨妊娠期肝内胆汁淤积症(ICP)患者胎盘凋亡调节基因表达水平与围生儿缺氧关系。 方法:以30例ICP 患者(ICP组)及27例正常产妇(对照组)为研究对象，应用免疫组化方法测定胎盘上凋亡调节基因bax和bcl-2的表达水平。结果:①ICP组围生儿缺氧的发生率显著高于对照组(43.33%vs.7.41%,P<0.005);②ICP组bax中等以上表达阳性率显著高于对照组(63.33%vs.18.52%,P<0.0005), 而bcl-2的表达水平低于对照组(60%vs.88.89%,P<0.0005);③围生儿缺氧风险有随着bax表达水平升高而增加的趋势(P<0.01)。结论：ICP患者胎盘合体滋养细胞bax基因过度表达，胎盘细胞凋亡率升高，影响胎盘功能，可能是ICP并发围生儿缺氧的病理生理基础之一。

　　【关键词】 胆汁淤积症(ICP)  妊娠并发症 滋养细胞 胎儿窘迫

　　The relationship between the perinatal hypoxia and placental apoptosis-associating gene expression in patients with intrahepatic cholestasis within pregnancy ZHAO Ya-juan, SONG xin (Department of Obstetrics and Gynecology,Taihe Hospital, Yunyang Medical college, Shiyan,Hubei 442000, China)

　　Abstract: Objective To explore the relationship between the expression level of apoptosis gene in placenta and perinatal hypoxia of patients with intrahepatic cholestasis within pregnancy (ICP). Methods Samples were obtained from 30 cases with ICP and 27 normal pregnant women(control group). Bax and bcl-2 level in placenta was detected by immunohistochemistry method. Results ①Perinatal hypoxia rate of ICP group was higher than that of the control group significantly (43.33%vs.7.41%, P<0.005). ②bax expression level in syncytiotrophoblast of ICP group was higher than that of the control(63.33%vs.18.52%,P<0.0005),and bcl-2 expression level was lower than the control(60%vs.88.89%,P<0.0005), both significantly. ③A increasing trend of perinatal hypoxia rate between bax expression level was found in our study(P<0.01). Conclusion One of the possible mechanism involved in perinatal of ICP is apoptosis caused by overexpression of bax in syncytiotrophoblast leading placental dysfunction.

　　Key words： pregnancy complications; cholestasis; apoptosis; bax; bcl-2; placenta

　　妊娠期肝内胆汁淤积症(intrahepatic cholestasis of pregnancy, ICP)的主要危害是引起胎儿窘迫，新生儿窒息及围生儿死亡率升高[1]，但其机制尚不清楚。有研究认为ICP患者胎盘病理改变与胎儿宫内缺氧有关[2]。胎盘上存在凋亡调节蛋白bax及bcl

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