Sağol Sermet, Sağol Ozgul, Ozkal Sermin, Asena Uçar
Department of Obstetrics and Gynecology, Ege University Medical Faculty, Department of Pathology, Dokuz Eylül University Medical Faculty, Izmir, Turkey.
J Reprod Med. 2002 Oct;47(10):809-15.
To examine the degree of apoptosis in human fetal membranes associated with premature rupture of membranes (PROM) as compared with normal pregnancies and to evaluate the expression of proapoptotic bax and antiapoptotic bcl-2 gene products.
Fetal membranes from 50 pregnancies were included in the study. Thirty of 50 pregnancies had PROM. Twenty pregnancies with intact membranes served as controls. Chorioamniotic membrane biopsies were taken from the rupture site of the membrane and periphery of the rupture side. In the control group, membrane biopsies were taken from the artificial rupture site, cervical pole of the membranes and membranes close to the edge of the placenta. In recognizing apoptotic figures, routinely processed samples were stained with hematoxylin and eosin for light microscopic evaluation. Quantification of the apoptotic cells was performed with high-power fields and expressed as the number per 100 cells. The membranes of both groups were then stained with bcl-2 and bax antibodies by using the standard steptavidin-biotin-immunoperoxidase method. Staining with both antibodies were compared between two groups.
Apoptotic cells were detected in the amniotic epithelium, in chorionic cells and fibroblastic layer of the fetal membranes. Apoptotic cells were found mostly in the chorionic cells. There was a statistically significant difference between the apoptotic index in PROM and the control group in both rupture and peripheral sites (P < .05), although within each group peripheral and rupture sites showed no difference in terms of apoptotic cell counts. Both bax and bcl-2 expression was observed in 40% of control cases and in 57% and 50% of cases with PROM, respectively, mostly in the chorionic trophoblastic cells. The PROM and control groups showed no statistically significant difference in terms of bcl-2 and bax protein expression.
Apoptosis may play a role in the pathogenesis of PROM, but the changes in apoptosis do not seem to be mediated by bcl-2 and bax genes in the amniotic membrane. Other regulatory mechanisms must be investigated.
与正常妊娠相比，研究胎膜早破（PROM）时人胎膜的凋亡程度，并评估促凋亡蛋白bax和抗凋亡蛋白bcl-2基因产物的表达。
本研究纳入了50例妊娠的胎膜。50例妊娠中有30例发生胎膜早破。20例胎膜完整的妊娠作为对照。从胎膜破裂部位及破裂侧周边取绒毛羊膜活检组织。对照组从人工破膜部位、胎膜宫颈极及靠近胎盘边缘的胎膜处取活检组织。为识别凋亡细胞，常规处理的样本用苏木精和伊红染色，进行光镜评估。在高倍视野下对凋亡细胞进行定量，并以每100个细胞中的数量表示。然后采用标准的链霉亲和素-生物素-免疫过氧化物酶法，用bcl-2和bax抗体对两组胎膜进行染色。比较两组抗体染色情况。
在羊膜上皮、绒毛膜细胞和胎膜的成纤维细胞层中检测到凋亡细胞。凋亡细胞主要存在于绒毛膜细胞中。胎膜早破组与对照组在破裂部位和周边部位的凋亡指数均有统计学显著差异（P <.05），尽管每组内周边部位和破裂部位的凋亡细胞计数无差异。在40%的对照病例以及分别在57%和50%的胎膜早破病例中观察到bax和bcl-2表达，主要在绒毛膜滋养层细胞中。胎膜早破组与对照组在bcl-2和bax蛋白表达方面无统计学显著差异。
凋亡可能在胎膜早破的发病机制中起作用，但羊膜中凋亡的变化似乎并非由bcl-2和bax基因介导。必须研究其他调节机制。
