摘要
目的:通过检测Ⅲ型胶原及TNF-α在胎膜早破患者胎膜组织中的表达,探讨二者在胎膜早破发病机制中的作用及其相互关系,分析推断足月胎膜早破(tPROM)与未足月胎膜早破(pPROM)的发病机制是否相同。方法:选取非足月胎膜早破组(pPROM)18例,足月胎膜早破组(tPROM)20例,选取与胎膜早破组孕周相对应的早产组(18例)和足月组(20例)分娩孕妇为对照组。均行剖宫产,胎盘胎膜娩出后避开自然破裂口或人工破口处取胎膜组织,常规HE染色在光镜下进行形态学观察,采用免疫组化法检测Ⅲ型胶原和TNF-α的表达情况,并进行直线相关分析。结果:①胎膜早破组胎膜组织完整性差,羊膜层和绒毛膜层分离现象多见,羊膜层胶原纤维及细胞外基质呈无序状态并减少。②4组胎膜组织中均有Ⅲ型胶原及TNF-α蛋白不同程度的阳性表达,Ⅲ型胶原主要定位于羊膜的ECM中,TNF-α主要定位于绒毛膜滋养细胞胞浆中。③Ⅲ型胶原在pPROM组、tPROM组的表达水平均低于对照组,差异有统计学意义(P<0.05),在pPROM组的表达亦低于在tPROM组,两者比较差异有统计学意义(P<0.01)。TNF-α在pPROM组、tPROM组的表达水平均高于相应对照组,差异有统计学意义(P<0.01),在pPROM组的表达低于在tPROM组,但无统计学差异(P>0.05)。④Ⅲ型胶原与TNF-α两者在tPROM组中的表达水平呈负相关性(r=-0.655,P<0.01),但两者在pPROM组中的表达水平无相关性(r=-0.385,P>0.05)。结论:①tPROM的发生可能与胎膜的退行性变及各种因素引发的胎膜细胞过度凋亡有关,而pPROM的发生更倾向于胎膜本身结构异常所致。②推断pPROM和tPROM两者是否有胎膜组织结构异常所导致的共同结果,但可能存在不同的机制。
Objective： To detect the expression of collagen Ⅲ and tumor necrosis factor （TNF） - αin fetal membranes of premature rupture of human fetal membranes （PROM） and non - PROM, to explore their roles and correlations in the etiology of PROM, and to analyze and deduce the different etiology of term PROM （tPROM） and preterm PROM （pPROM） . Methods： 18 cases of pPROM and 20 cases of tPROM and 20 eases of premature deliveries and 20 cases of term deliveries were selected. All the fetal membranes was immediately taken from the site which was far away from the rupture membranes after cesarean section. The samples were staining with hematoxylin and eosin （HE） for morphology observation. The collagenⅢ and TNF- α.levels were detected with streptavidin peroxidase biotin （SP） immuno- histochemistry was made and the linear correlation analysis was conducted. Results： ①The integrity of the fetal membranes were poor, amnion epithelial cell and the basement membranes presented diasocidtion pheaomend, the fibrillar collagen and amnion extracellular matrix （ECM） were disordered state and deceased in pPROM group. ②The expression of collagenⅢ and TNF - ct with different levels was seen in fetal membranes of the four groups. CollagenⅢ was major fixed in the ECM of amnion and TNF - αwas expressed in ehorion trophocyte. ③In pPROM group and tPROM group, collagen Ⅲ were all decreased significantly compared to those of the corresponding control groups （ P 〈 0. 05）. Less expression of collagen Ⅲ was found in pPROM than that in tPROM group （P 〈 0. 01 ）. The expression of TNF-α in pPROM and tPROM group increased significantly compared with those of the corresponding control groups （ P 〈 0. 01 ）. The level of TNF - α was lower in pPROM than that of tPROM, but had no significance （P 〉 0. 05） .④For tPROM pregnant women, collagen Ⅲ was negatively correlated with TNF - α （ r = - 0. 655, P 〈 0. 01 ）. But no correlation was found in pPROM pregnant women （ r = - 0. 385, P 〉 0. 05） . Conclusion： ①The cause of tPROM is probably related with the degeneration of fetal membranes and the various factors induced excessive apoptosis. The reasons of pPROM are probably prone to the disorder of fetal membranes.②There might be the same results that lead to the abnormality of fetal membranes construction between pPROM and tPROM, however the mechanism is different.
出处
《中国妇幼保健》
CAS
北大核心
2008年第33期4756-4759,共4页
Maternal and Child Health Care of China
基金
河南省科技攻关项目(2005158057)
关键词
胎膜早破
Ⅲ型胶原
TNF—α
免疫组化
Premature rupture of human fetal membranes
Ⅲ type collagen
Tumor necrosis factor - α
Immunohistochemistry
