Cx43、Bax和Bcl-2在胎膜早破患者胎膜组织中的表达及意义

目的检测间隙连接蛋白43（Cx43）在胎膜早破患者胎膜组织中的表达，分析其与凋亡相关蛋白Bax、Bcl-2表达的相关性，探讨三者与胎膜早破发生的关系。方法随机选择本院剖宫产分娩的孕32-42周胎膜早破孕妇30例（胎膜早破组），其中未足月胎膜早破（pPROM）15例，足月胎膜早破（tPROM）15例；无胎膜早破孕妇30例（对照组）。采用免疫组化法（PV法）检测Cx43、Bax和Bcl-2的表达并进行图像分析。结果①各组胎膜组织中均可见Cx43、Bax、Bcl-2不同程度的表达。②tPROM组Cx43、Bcl-2的表达明显低于对照组（P〈0．01），而Bax的表达高于对照组，差异均有显著性（P〈0．05）。tPROM组Cx43的表达高于pPROM组，差异有显著性（P〈0．01）；而Bcl-2、Bax在两组中比较，差异无显著性（P〉0．05）。③PROM组人工胎膜破口附近Cx43、Bcl-2的表达低于非人工胎膜破口附近，Bax的表达则相反，两组比较，差异有显著性（均P〈0．01）。④PROM组Cx43的表达水平与Bax呈负相关（r=-0．309，P〈0．05）。结论胎膜组织中Cx43的低表达及细胞的过度凋亡可能对胎膜早破的发生起一定的促进作用。

Expression of connexin 43,Bax and Bcl-2 on human fetal membranes of premature rupture of membranes

Objective To examine the expression of connexin 43 （Cx43） and its relationship with the expres- sion of apoptosis related proteins, Bax and Bel-2, on fetal membranes of premature rupture of membranes （PROM）. Methods Fetal membranes from 60 cesarean section deliveries at gestational age of 32 to 42 weeks were recruited in the study, 15 from preterm delivery with PROM （pPROM）, 15 from term delivery with PROM （tPROM） and 30 non- PROM deliveries served as control group. Expression of Cx43, Pax and Bcl-2 on fetal membranes was detec- ted immunohistochemically and analyzed by computer image analysis system. Results （1） Expression of Cx43, Bax and Bel-2 were detectable on the fetal membranes of all groups. （2） In tPROM group, expression of Cx43 and Bcl-2 were significantly less than in the control group （P〈0. 01）, and Pax expression was more than in the control group （P〈0. 05）. In tPROM group, expression of Cx43 was more than that in pPROM group （P〈0. 01）, but no significant difference was found in expression of Bcl-2 or Pax between the two groups （P〉0. 05）. （3） In PROM group, expression of Cx43 and Bel-2 were less and Bax expression was more at the rupture site than 10 cm from the rupture site of uterine - incision delivery （P〈0. 01）,（4） In PROM group, negative correlation was found between Cx43 and Pax expression （r=- 0. 309, P〈0. 05）. Conclusion The decreases of Cx43 expression and excessive apoptosis in fetal membranes may play an important role in PROM.