水通道蛋白9在人胎盘和胎膜中的表达

目的 检测正常人胎盘与胎膜中水通道蛋白9（aquaporin 9，AOP9）的表达。方法 收集5例足月剖宫分娩的胎盘和胎膜样本，运用RT—PCR方法从mRNA水平检测AQP9在胎盘与胎膜的表达；运用免疫组织化学和Western印迹方法检测AQP9蛋白在胎盘与胎膜中的表达。结果 RT—PCR结果显示AQP9mRNA在胎盘和胎膜均有表达；Western印迹显示两条带在相对分子量为30kD及45kD左右；免疫组织化学显示AQP9表达于胎盘的合体滋养细胞、羊膜上皮细胞及平滑绒毛膜滋养细胞。结论 AQP9在母胎液体交换、胎儿代谢物的排出及羊水平衡等的分子机制中可能发挥重要作用。     

水通道蛋白1和水通道蛋白3在羊水过少孕妇胎盘和胎膜的表达及其意义

Objective To study the expression of aquaporin 1 (AQP1) and aquaporin 3 (AQP3) in fetal membranes and placenta in pregnant women with oligohydramnios and to explore their function in the balance of amniotic fluid. Methods Thirty cases of term pregnancy with oligohydramnios were selected as the experimental group and 30 healthy term pregnant women with normal amniotic fluid volume were served as control. The expressions of mRNA and protein of AQP1 and AQP3 in fetal membranes and placenta were examined by real-time polymerase chain reaction and streptavidi peroxidase immunohistochemiscal staining. Results The expression of AQP1 mRNA in the amnion of the experimental group was 0.31 relative to that of the control group. The expression of AQP1 protein in the amnion of the experimental group was 0.14±0.02, which showed significant decrease when compared with the control (0.25±0.03) (P<0.05), while no significant difference in the chorion and placenta was found between the two groups(P>0.05). The amount of AQP3 mRNA expressions in amnion and chorion in the experimental group were 0.31 and 0.37 relative to those of the control group, respectively, while 7.36 in the placenta. The expression of the AQP3 protein in the amnion and chorion in the experimental group were 0.18±0.05 and 0.18±0.04, respectively, which showed significant decrease when compared with those in the control group (0. 26±0.03 vs 0.29± 0.06, P<0.05). But the expression of AQP3 protein in the placenta of experimental group was significantly higher than that of the control (0.47±0.09 vs 0.28±0.01, P<0.05). Conclusions The alterations of AQP1 and AQP3 expressions in fetal membrane and placenta in oligohydramniotic women are adaptive response to oligohydramnios.     

水通道蛋白1和水通道蛋白3在羊水过少孕妇胎盘和胎膜的表达及其意义

目的 研究水通道蛋白1(AQP1)和AQP3在羊水过少孕妇胎盘、胎膜中的表达及分布,探讨其在羊水平衡途径中的作用. 方法 选取30例孤立性羊水过少的足月孕妇为研究组,同期分娩的30例正常羊水量的足月孕妇为对照组.分别采用实时荧光定量PCR和免疫组织化学SP法,检测两组胎盘、胎膜组织中AQP1和AQP3 mRNA和蛋白的表达及分布. 结果 AQP1mRNA在研究组羊膜组织中的表达为对照组的0.31,AQP1蛋白在研究组羊膜组织中的表达为0.14±0.02,较对照组的0.25±0.03明显下调(P<0.05).而在胎盘、绒毛膜中的分布及表达强度两组间差异无统计学意义(P>0.05).AQP3 mRNA在研究组羊膜和绒毛膜中的表达分别为对照组的0.31和0.37,而胎盘中的表达为对照组的7.36.AQP3蛋白在研究组羊膜和绒毛膜中的表达分别为0.18±0.05和0.18±0.04,均较对照组的0.26±0.03和0.29±0.06明显下调(P<0.05),而在胎盘组织中的表达研究组为0.47±0.09,较对照组0.28±0.01明显上调(P<0.05). 结论 AQP1和AQP3在羊水过少孕妇胎盘、胎膜组织中表达的改变为羊水减少后的代偿性反应.     

Expression of aquaporin 9 in human chorioamniotic membranes and placenta

OBJECTIVE: Aquaporin 9 (AQP9) is one of the recently identified water channels that is also permeable to neutral solutes including urea. To investigate the molecular mechanism of intramembranous pathway of amniotic fluid regulation, we sought to determine whether AQP9 is expressed, and the cellular localization of AQP9 expression in human fetal membranes. STUDY DESIGN: Fetal membranes from 5 normal term human pregnancies were studied. Northern analysis was used to determine the tissue AQP9 messenger RNA (mRNA) expression. In situ hybridization and immunohistochemical staining with specific anti-AQP9 antibody was used for cellular AQP9 localization in the human fetal membranes. RESULTS: Northern analysis detected AQP9 mRNA expression in human amnion, chorion, and placenta. In situ hybridization revealed AQP9 mRNA expression in epithelial cells of the amnion, chorion cytotrophoblasts, and syncytiotrophoblasts and cytotrophoblasts of placenta. Further immunohistochemical study confirmed the AQP9 protein expression in these cell types of fetal membranes. CONCLUSION: This study demonstrated the expression of AQP9 mRNA and protein in human chorioamniotic membranes and placenta. The AQP9 expression in fetal membranes suggests that AQP9 may be an important water channel in intramembranous amniotic fluid water regulation.     

Expression and localization of cell adhesion molecules in human fetal membranes during parturition

There is increasing evidence to support the view that human parturition represents an inflammatory process. We have previously demonstrated that parturition is associated with leukocyte invasion and pro-inflammatory cytokine production in the cervix and myometrium. Furthermore, we have shown that several cell adhesion molecules are upregulated in these tissues during labor. In fetal membranes, previous studies have shown intercellular adhesion molecule-1 (ICAM-1) upregulation in association with labor. The role of other adhesion molecules has not been explored. The aims of this study were, therefore, to determine the expression of ICAM-1, platelet endothelial cell adhesion molecule (PECAM), vascular cell adhesion molecule (VCAM) and E-selectin in pre- and post-laboring amnion and choriodecidua and to identify cell types responsible for their expression. Biopsies of fetal membranes were obtained from pregnant women delivered by caesarean section before the onset of labor (n = 8) and following spontaneous vaginal delivery (n = 8). Cell adhesion molecules were identified using immunohistochemistry and messenger RNA expression quantified using Northern analysis. We found that following labor, ICAM-1 mRNA expression was significantly upregulated in amnion and choriodecidua (P < 0.05). PECAM mRNA expression was also increased in choriodecidua (P < 0.05). The main cell types responsible for adhesion molecule expression were leukocytes, amniotic epithelial cells and endothelial cells. The upregulation of ICAM-1 and PECAM mRNA expression in fetal membranes following labor provides further evidence that fetal membranes play an important role in the inflammatory process of parturition.     

水通道蛋白3、9在特发性羊水过多产妇胎盘和胎膜中的表达变化及意义

目的 探讨水通道蛋白(AQP)3、9在特发性羊水过多产妇胎盘和胎膜中的表达、分布及其在特发性羊水过多发病巾的作用.方法 2006年6月至2008年3月,选择在温州医学院附属第二医院产科住院并分娩的21例特发性羊水过多的足月产妇为研究组,同期分娩的30例羊水量正常的足月产妇为对照组.采用实时荧光定量PCR技术,检测两组产妇胎盘、胎膜中AQP3、9 mRNA的表达及分布,采用免疫组化链霉菌抗生物素蛋白.过氧化物酶(SP)连接法枪测两组产妇胎盘、胎膜中AQP3、9蛋白的表达及分布.结果 (1)两组产妇羊膜、绒毛膜、胎盘中均可检测到AQP3、9 mRNA的表达.AQP3、9主要表达于羊膜上皮细胞、绒毛膜滋养细胞、胎盘滋养细胞.(2)研究组羊膜上皮细胞AQP3、9 mRNA的表达分别为对照组的5.00倍和3.25倍,而研究组绒毛膜滋养细胞AQP3、9 mRNA的表达分别为对照组的2.03倍和2.08倍,分别比较,差异均有统计学意义(P<0.01);但是研究组胎盘滋养细胞AQP3、9 mRNA的表达均明显低于对照组,差异也有统计学意义(P<0.01).(3)AQP3、9蛋白在研究组羊膜上皮细胞的表达强度为7.5±2.0、11.1±1.8,对照组为5.3 ±1.6、5.6±2.3,两组比较,差异有统计学意义(P<0.05);AQP3、9蛋白在研究组绒毛膜滋养细胞的表达强度为7.5±2.0、10.0±1.6,对照组为5.4±2.2、5.6±2.1,分别比较,差异也有统计学意义(P<0.05),但是AQP3、9蛋白在胎盘滋养细胞的表达强度(3.5±1.4、4.0 ±2.5)较对照组(5.6±1.3、7.1±2.9)明显下调(P<0.05).结论 AQP3、9在特发性羊水过多产妇胎盘和胎膜中的表达变化可能为羊水增加后的代偿性反应,其调节机制尚待进一步研究.     

原发性羊水过多产妇胎膜和胎盘组织中水通道蛋白8的表达

目的 探讨水通道蛋白8(AQP8)在原发性羊水过多产妇胎膜和胎盘组织中的表达.方法 收集2005年10月-2007年5月重庆医科大学附属第一医院和重庆市妇幼保健院行足月剖宫产分娩(孕37～40周)的原发性羊水过多产妇12例为羊水过多组,同期因社会因素行剖宫产分娩的正常产妇12例为对照组.采用RT-PCR技术检测两组产妇胎膜和胎盘组织中的AQP8 mRNA表达水平;采用免疫组化技术检测两组产妇胎膜和胎盘组织中的AQP8蛋白表达水平.结果 (1)羊水过多组羊膜、绒毛膜和胎盘组织中的AQP8 mRNA表达水平分别为0.78±0.13、0.58±0.10、0.86±0.15,对照组分别为0.39±0.07、0.45±0.09、0.34±0.09,羊水过多组各组织中AQPS mRNA表达水平均高于对照组,两组分别比较,差异均有统计学意义(P<0.05).(2)羊水过多组羊膜、绒毛膜和胎盘组织中的AQP8蛋白表达水平分别为0.195±0.024、0.170±0.028、0.193±0.024,对照组分别为0.151±0.018、0.156±0.024、0.152±0.023,其中羊水过多组羊膜、胎盘组织中AQP8蛋白表达水平均高于对照组,差异有统计学意义(P<0.05),而羊水过多组绒毛膜组织中AQP8蛋白表达水平虽高于对照组,但两组比较,差异无统计学意义(P>0.05).结论 原发性羊水过多产妇羊膜和胎盘组织中AQP8mRNA及蛋白的表达水平均显著高于正常产妇,提示AQP8在产妇羊水量的调节中发挥重要作用.     

Expression and localisation of FoxO3 and FoxO4 in human placenta and fetal membranes

Forkhead box O (FoxO) proteins regulate inflammation, extracellular matrix (ECM) remodelling and apoptosis. We have previously identified FoxO1 proteins in human gestational tissues, and demonstrated a link between FoxO1 and rupture of fetal membranes. There is, however, no data available on the expression and localisation of FoxO3 and FoxO4 in human intrauterine tissues. Thus the aim of this study was to characterise the localisation and expression of FoxO3 and FoxO4 in (i) human placenta and fetal membranes before term spontaneous labour onset, and (ii) supracervical site (SCS) and distal site (DS) fetal membranes from non-labouring women. Immunohistochemistry, Western blotting and quantitative RT-PCR (qRT-PCR) was used to localise and quantitate FoxO3 and FoxO4 protein and mRNA expressions. Cytoplasmic and nuclear FoxO3 was localised in the syncytiotrophoblast layer, chorionic trophoblasts, amnion epithelium and decidua. Cytoplasmic FoxO4 was localised in the syncytiotrophoblasts and chorionic trophoblasts. No or very little FoxO4 protein and mRNA was present in amnion epithelium. The intensity and extent of staining of FoxO3 and FoxO4 was greater in fetal membranes obtained from the SCS compared to DS. Presence of FoxO3 and FoxO4 are expected to contribute to apoptosis and/or cell cycle regulation associated with fetal membrane rupture.     

Expression and cellular localisation of chloride intracellular channel 3 in human placenta and fetal membranes

Chloride channels regulate the movement of a major cellular anion and are involved in fundamental processes that are critical for cell viability. Regulation of intracellular chloride is achieved by multiple classes of channel proteins. One class of putative channels are the chloride intracellular channel (CLIC) family. Evidence suggests that several CLICs are expressed in human placenta, although their roles in this tissue are not certain. Northern blot analysis has shown that CLIC3 is highly expressed in placenta relative to other human tissues; however, its cellular distribution is not known. This study used microarray expression profiling to clarify which CLICs are expressed in human placenta and RT-PCR, Western blot and immunohistochemistry to determine the expression pattern of CLIC3 in human placenta and fetal membranes. Placentas and fetal membranes were obtained from term pregnancies after delivery and placental tissue was obtained from first trimester following either chorionic villous sampling or elective pregnancy termination. Trophoblast cells were isolated from first trimester and term placentas and placental endothelial cells were isolated from term placentas. Microarray expression profiling identified high expression of mRNA for CLICs 1, 3 and 4 in the isolated first trimester and term trophoblast cells. High mRNA expression in the isolated endothelial cells was also found for CLICs 1 and 4, but not CLIC3. Low expression was found for CLIC5 in all three types of isolated cells. RT-PCR confirmed that CLIC3 mRNA was expressed in trophoblast cells at both gestational ages, but was not present in endothelial cells. CLIC3 mRNA was also identified in whole placental extracts at both gestational ages and in term amnion and choriodecidua. Immunohistochemistry using a chicken anti-human CLIC3 antibody localised strong CLIC3-specific staining to the syncytiotrophoblast and villous cytotrophoblast cells in both first trimester and term placentas, and weaker staining in extravillous trophoblast cells in first trimester. In fetal membranes at term strong CLIC3-specific staining was localised to chorionic trophoblast cells, with weaker staining in amniotic epithelial and decidual cells. It was previously shown that chloride uptake was increased into cells that had been transfected with CLIC3. CLIC3 may facilitate chloride ion movement and the regulation of cellular processes associated with the movement of chloride in the placental and fetal membrane cells in which it is expressed.     

水通道蛋白3在人羊膜上皮细胞中的表达及调控

目的 研究丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPK)/细胞外信号调节激酶(extracellular signal regulated kinase,ERK)信号转导通路对人羊膜上皮细胞中水通道蛋白3(aquaporin,AQP3)表达的调控作用. 方法 选择2011年1月至11月,在温州医学院附属第二医院产科分娩的不明原因羊水过少和羊水量正常的足月单胎妊娠产妇各10例,均为剖宫产分娩.原代培养羊膜上皮细胞,并用ERK1/2抑制剂U0126进行处理.浓度为0、5、10、20和40 μmol/L的U0126分别作用12 h;再选取使磷酸化ERK1/2表达水平最低的浓度为最佳浓度,作用于细胞0、2、6、12和24 h.采用免疫细胞化学染色检测AQP3蛋白定位,Western印迹检测总ERK1/2、磷酸化ERK1/2和AQP3蛋白表达水平.统计学方法采用t检验和方差分析. 结果 (1)羊水过少组磷酸化ERK1/2和AQP3的表达均低于羊水量正常组(ERK1/2:2.46±0.25与3.46±0.33;AQP3:1.56±0.10与2.34±0.18,t=9.243和13.292,P＜0.01).(2)羊水过少组中U0126不同浓度组间比较,总ERK1/2表达差异无统计学意义(F=0.365,P＞0.05);5、10、20、40 μmol/L组磷酸化ERK1/2和AQP3表达均低于0μmol/L组(磷酸化ERK1/2:0.96±0.16、1.12±0.13、0.98±0.17、1.02±0.26与2.46±0.25; AQP3:1.10±0.09、1.12±0.08、1.13±0.06、1.11±0.06与1.56±0.10,P＜0.05);但5μmol/L组与10、20和40 μmol/L组比较,差异均无统计学意义(P＞0.05).羊水过少组U0126作用的最佳浓度为5 μmol/L.该浓度作用2h组磷酸化ERK1/2和AQP3表达均低于0h组(磷酸化ERK1/2:1.27±0.29与2.55±0.12;AQP3:1.44±0.12与2.15±0.09,P＜0.05),但2h组与6、12和24 h组比较,差异均无统计学意义(P＞0.05).最佳作用时间为2h.(3)羊水量正常组和羊水过少组产妇的羊膜上皮细胞中,胞浆及胞膜均有AQP3蛋白阳性染色,但主要位于胞浆.U0126作用后,AQP3蛋白在羊膜上皮细胞中定位无明显改变. 结论 U0126可抑制羊水过少者的羊膜上皮细胞ERK1/2磷酸化及AQP3蛋白表达,提示MAPK/ERK1/2信号转导通路可能对羊膜上皮细胞中AQP3蛋白表达起调控作用,从而影响羊水量的平衡.     

Expression of natural antimicrobials by human placenta and fetal membranes

Preterm birth associated with infection is a major clinical problem. We hypothesized that this condition is associated with altered expression of natural antimicrobial molecules (beta-defensins (HBD), elafin). Therefore, we examined expression of these molecules and their regulation by proinflammatory cytokines in placentae and fetal membranes from term pregnancy. HBD1-3 and elafin were localized by immunohistochemistry in fetal membranes and placenta. Real-time quantitative PCR was used to examine mRNA expression in primary trophoblast cells treated with inflammatory molecules. HBD1-3 and elafin were immunolocalized to placental and chorion trophoblast layers of fetal membranes and placenta. Immunoreactivity was also observed in amnion epithelium and decidua. No differences were noted between samples from women who were not in labour compared to those in active labour. In in vitro cultures of primary trophoblast cells, HBD2 and elafin mRNA expression was upregulated by the proinflammatory cytokine, IL-1beta. These results suggest that the chorion and placental trophoblast layers may be key barriers to the progression of infection in the pregnant uterus. Natural antimicrobial expression may be altered in response to inflammatory mediator expression associated with the onset of labour and/or uterine infection, providing increased protection when the uterus may be particularly susceptible to infection.     

Role of aquaporin 1 in fetal fluid homeostasis

Abstract

Introduction: The homeostasis of maternal-fetal fluid exchange is critically important in pregnancy. We sought to investigate the function of aquaporin 1 (AQP1) during pregnancy by examining fluid compartments of AQP1 knockout (AQP1-KO) mice.

Methods: Homozygous pregnant AQP1 knockout (KO) mice and control pregnant wild type CD1 mice were sacrificed. Placenta and fetal membranes were examined by immunohistochemical staining for expression of AQP1. The total number of embryos, atrophic embryos, and fetal and placental weight was recorded in each subgroup. Amniotic fluid amount in each sac was measured and amniotic fluid composition was determined. Analysis of variance of factorial design and one-factor analysis of variance were used for statistics.

Results: Immunohistochemistry performed on CD1, though not AQP1-KO, placenta revealed that AQP1 was expressed at the vascular endothelial cell, trophocyte, and amnion epithelial cell. In AQP1-KOs, the number of embryos decreased with advancing gestational age. Although the fetal weight of AQP1-KO mice was significantly lower than wild type, amniotic fluid amount was increased in AQP1-KO mice. The AQP1-KO placenta demonstrated increased degeneration with evidence of altered blood vessel structure and increased syncytiotrophoblast nodules.

Conclusions: These findings demonstrate a critical role of AQP1 in placental and fetal growth and maternal-fetal fluid homeostasis.     

Expression of GLUT12 in the fetal membranes of the human placenta

The aim of this study was to characterize the expression of the novel glucose transporter GLUT12 in the fetal membranes of the human placenta. RT-PCR and Western blotting of extracts of amnion and choriodecidua from four normal term placentas identified GLUT12 mRNA and protein expression. In all four samples the signals for GLUT12 were markedly stronger in the choriodecidua than in the amnion, whereas the signals for GLUT1, a glucose transporter know to be expressed in fetal membranes, were similar for the two tissues. In further studies, paraffin sections of fetal membranes were analyzed by immunohistochemistry with GLUT12 and GLUT1-specific polyclonal antibodies. GLUT12 immunoreactivity was localized predominantly to the trophoblast cells in the chorion and to a lesser extent to decidual cells and to epithelial and fibroblast cells of the amnion. GLUT1 was localized to chorionic trophoblast cells and amniotic epithelial and fibroblast cells. GLUT12 expression was predominantly cytoplasmic, whereas GLUT1 was associated with the membrane of the cells. These results show that GLUT12 is expressed in cells of human fetal membranes and suggest that GLUT12 may play a role in the facilitation of glucose transport into these cells.     

Biomechanical characteristics of human fetal membranes. Preterm fetal membranes are stronger than term fetal membranes

The purpose of this study was to determine the biomechanical characteristics of human fetal membranes (FM) throughout gestation. Biomechanical properties were determined for 115 FM of 23-41 weeks gestation using our previously described methodology. The areas of membrane immediately adjacent to the strongest and weakest tested spots were sampled for histomorphometric analysis. Clinical data on the patients whose FM were examined were also collected. FM less than 28 weeks gestation were associated with higher incidence of abruption and chorioamnionitis. Topographically FM at all gestations had heterogeneous biomechanical characteristics over their surfaces with distinct weak areas. The most premature membranes were the strongest. FM strength represented by rupture force and work to rupture decreased with increasing gestation in both weak and strong regions of FM. This decrease in FM strength was most dramatic at more than 38 weeks gestation. The FM component amnion-chorion sublayers were thinner in the weak areas compared to strong areas. Compared to term FM, preterm FM are stronger but have similar heterogeneous weak and strong areas. Following a gradual increase in FM weakness with increasing gestation, there is a major drop-off at term 38 weeks gestation. The FM weak areas are thinner than the stronger areas. Whether the difference in thickness is enough to account for the strength differences is unknown.     

Ontogeny of aquaporins 1 and 3 in ovine placenta and fetal membranes

A sensitive and highly reproducible method has been used to show that Aquaporin 3 (AQP(3)) mRNA is present in the ovine placenta and chorion from at least 60 days of gestation (term=145-150d) with levels increasing substantially (>16 fold) at 100 days, and remaining constant thereafter. By immuno- and hybridization histochemistry, the epithelial cells expressing AQP(3)were found to be the trophoblast cells. Some AQP(3)was expressed in fibroblasts of the amnion and allantois but none was expressed in the epithelia of these membranes. AQP(1)was expressed in endothelial cells of fetal and maternal blood vessels but not in any epithelial cell of the ovine placenta and fetal membranes. The level of AQP(3)expression is consistent with known ovine placental permeabilities to water, glycerol and urea.     

Proteoglycans and hyaluronan in human fetal membranes

OBJECTIVE: The aim of this study was to describe the distributions of major extracellular matrix components, such as proteoglycans, collagen and hyaluronan, in the fetal membranes at term.Study Design: Fetal membranes were obtained from elective cesarean deliveries at term. Guanidinium extracts were analyzed for proteoglycans with alcian blue precipitation, sodium dodecyl sulfate- polyacrylamide gel electrophoresis, and Western blotting and for hyaluronan with a radioimmunoassay. Collagen was measured by estimating hydroxyproline content. Tissue sections were immunostained for decorin and biglycan and stained for hyaluronan with a biotin-labeled hyaluronan-binding protein. RESULTS: The fetal membranes contained predominantly smaller proteoglycans, such as biglycan and decorin. The amnion consisted of typical fibrous connective tissue with a high concentration of collagen. The amnion was dominated by decorin located in close connection with the collagen fibrils. The chorion was composed of a fibroblastic part containing collagen and decorin and a trophoblastic part mainly containing biglycan. In addition, large amounts of hyaluronan were found, especially in the amnion and in the decidual cell layers. CONCLUSION: The distributions of proteoglycans, collagen, and hyaluronan in human fetal membranes may explain the biomechanical properties of this tissue. We suggest that changes in the relative proportions of these extracellular molecules are crucial for the proposed maturation process in the fetal membranes during the last weeks of pregnancy.     

血清TGF-β1、VEGF、HIF-1α在子宫内膜息肉患者中的表达及与息肉切除术后宫腔粘连关系

Objective?To study the expression of serum Transforming growth factor β1 (TGF-β1), Vascular endothelial cell growth factor (VEGF), hypoxia inducible factor 1α (HIF-1α) in endometrial polyps and their relationship with intrauterine adhesion after polypectomy. Methods?150 cases of patients with intrauterine polyps admitted to our hospital from January 2020 to January 2022 were selected for this study. According to postoperative follow-up, they were divided into adhesion group (n=65) and control group (n=85) without intrauterine adhesion. The expressions of TGF-β1, VEGF and HIF-1α in serum of the two groups were compared. Multivariate logistic regression was used to analyze the risk factors of endometrial adhesion after endometrial polyp surgery. Results?The levels of serum TGF-β1, VEGF and HIF-1α in adhesion group were significantly higher than those in control group (P<0.05). Univariate analysis showed that there was no significant difference in age, BMI, birth time, history of induced labor and uterine fibroids between two groups (P>0.05). Pregnancy, cesarean section, curettage, endometrial hyperplasia, pelvic inflammatory disease, IUD history, serum TGF-β1, VEGF, HIF-1α were correlated with endometrial adhesion after endometrial polyp (P<0.05). Multivariate non-conditional Logistic analysis showed that pregnancy, cesarean section, curettage history, endometrial hyperplasia, pelvic inflammatory disease history, intrauterine device history, serum TGF-β1, VEGF, HIF-1α increase were independent risk factors for endometrial polyp postoperative intrauterine adhesion. Conclusion?The high expression of serum TGF-β1, VEGF and HIF-1α in endometrial polyps may increase the risk of endometrial adhesion after endometrial polyps.     

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。