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1.
目的:检测中性粒细胞明胶酶相关载脂蛋白(NGAL)和基质金属蛋白酶-9(MMP-9)在卵巢上皮性肿瘤组织和血清中的表达,了解两者与卵巢癌临床病理特征的关系。方法:应用半定量RT-PCR和ELISA法检测50例上皮性卵巢癌、21例卵巢良性肿瘤和18例正常对照的卵巢组织和血清中NGAL和MMP-9的表达水平。结果:(1)卵巢癌组的组织及血清中NGAL和MMP-9表达明显高于卵巢良性肿瘤组和正常对照组(P均<0.05);二者的高表达与临床分期、淋巴结转移正相关(P均<0.05);卵巢癌患者的组织及血清中NGAL与卵巢癌的组织分化程度正相关(P均<0.05),MMP-9则与卵巢癌的组织分化程度负相关(P均<0.05)。(2)卵巢癌患者的组织或血清中,NGAL表达均与MMP-9表达呈正相关(r=0.740,r=0.676,P均<0.05)。结论:NGAL和MMP-9在卵巢上皮性癌中表达上调,可能与卵巢上皮性癌的发生、发展有关。  相似文献   

2.
目的:探讨HtrA1(high temperature requirement A1)在子痫前期孕妇血清、胎盘组织中的表达及意义。方法:HtrA1属分泌型蛋白,可采用酶联免疫吸附法(ELISA)测定同期住院孕妇的空腹血清HtrA1浓度,其中正常晚期妊娠30例、轻度子痫前期25例、重度子痫前期20例;同时应用免疫组化SABC法检测胎盘组织中HtrA1的表达。结果:正常晚期妊娠、轻度子痫前期及重度子痫前期孕妇血清HtrA1浓度分别为(160.63±32.52)pg/ml、(210.82±32.52)pg/ml及(233.68±38.61)pg/ml,组间差异显著(P<0.05);正常晚期妊娠、轻度子痫前期及重度子痫前期孕妇胎盘组织中HtrA的平均灰度值分别为156.03±5.07、149.89±2.69及140.05±4.96,组间差异显著(P<0.05)。结论:随着病情加重,孕妇血清及胎盘组织中HtrA1的表达显著增高。HtrA1与子痫前期的发生、发展有关。  相似文献   

3.
目的探讨胎盘滋养细胞中KiSS-1基因及基质金属蛋白酶(MMP)9在子痫前期发病中的作用及其与新生儿预后的相关性。方法采用RT-PCR和western blot(蛋白印迹法)检测40例子痫前期患者(其中轻度15例、重度25例,子痫前期组)和20例正常足月正常妊娠妇女(正常妊娠组)胎盘滋养细胞中KiSS-1mRNA和MMP-9mRNA及其蛋白的表达,并与其临床症状及其新生儿围产结局进行相关性分析。结果(1)子痫前期组滋养细胞中KiSS-1mRNA及其蛋白表达水平分别为1.73±0.24和(78.4±8.0)μg/100μg总蛋白,其中轻度患者为1.50±0.15和(72.4±6.9)μg/100μg总蛋白,重度患者为1.87±0.20和(83.5±3.6)μg/100μg总蛋白;均显著高于正常妊娠组的1.24±0.25和(63.4±2.7)μg/100μg总蛋白(P<0.01)。(2)子痫前期组MMP-9mRNA及其蛋白表达水平分别为0.09±0.06和(9.6±4.3)μg/100μg总蛋白,其中轻度患者为0.11±0.08和(10.0±3.2)μg/100μg总蛋白,重度患者为0.07±0.05和(7.8±2.0)μg/100μg总蛋白;均显著低于正常妊娠组的0.17±0.10和(17.9±7.3)μg/100μg总蛋白(P<0.01)。(3)子痫前期组KiSS-1mRNA及其蛋白表达水平与中心动脉压(MAP)和24h尿蛋白定量呈正相关,r分别为0.610(P=0.023)、0.713(P=0.011)和0.397(P=0.003)、0.638(P=0.002);与有、无眼底动脉痉挛呈显著正相关,r分别为0.499(P=0.000)和0.511(P=0.000)。子痫前期组MMP-9mRNA及其蛋白表达水平则与MAP、24h尿蛋白定量及有、无眼底动脉痉挛呈显著负相关,r分别为0.561(P=0.042)、0.571(P=0.022)、0.275(P=0.039)、0.375(P=0.048)、0.346(P=0.001)、0.543(P=0.000)。(4)子痫前期组MMP-9mRNA及其蛋白表达水平与新生儿体重呈显著正相关,r分别为0.651(P=0.000)和0.544(P=0.004);KiSS-1mRNA及其蛋白表达水平与其呈显著负相关,r分别为0.759(P=0.000)和0.865(P=0.000)。(5)随着新生儿窒息程度加重,MMP-9mRNA及其蛋白表达水平呈降低趋势,KiSS-1mRNA及其蛋白表达水平呈升高趋势(P均<0.05)。结论MMP-9和KiSS-1表达失衡在子痫前期发病中起重要作用,且与新生儿预后密切相关。  相似文献   

4.
目的探讨细胞外基质金属蛋白酶诱导因子(EMMPRIN)在子痫前期及子痫患者胎盘组织中的表达及其与子痫前期及子痫发病的关系。方法采用免疫组化链霉菌抗生物素蛋白-过氧化酶连接法和RT-PCR技术检测不同孕周的44例子痫前期(重度)孕妇(子痫前期组)、38例子痫孕妇(子痫组)和49例正常孕妇(正常妊娠组)胎盘组织中EMMPRIN蛋白及mRNA的表达。结果(1)EMMPRIN蛋白阳性表达:子痫前期组EMMPRIN蛋白表达中度阳性率为18%(8/44),强阳性率为9%(4/44);子痫组EMMPRIN蛋白中度阳性率为21%(8/38),强阳性率为13%(5/38),两组分别比较,差异均无统计学意义(P>0.05)。正常妊娠组EMMPRIN蛋白表达中度阳性率为12%(6/49),强阳性率为82%(40/49),与子痫前期组及子痫组比较,差异均有统计学意义(P<0.001)。(2) EMMPRIN mRNA表达:子痫前期组孕晚期(37~40周)EMMPRIN mRNA为0.342±0.002,子痫组为0.344±0.023,两组比较,差异均无统计学意义(P>0.05)。正常妊娠组孕晚期(37~40周) EMMPRIN mRNA为0.872±0.094,分别与子痫前期组及子痫组比较,差异均有统计学意义(P<0.001)。结论子痫前期及子痫患者胎盘组织中EMMPRIN表达水平下降是子痫前期及子痫发病的重要原因;EMMPRIN可作为子痫前期及子痫发病的一个预测指标。  相似文献   

5.
妊娠期高血压疾病(PIH)的发病机制尚不明确,目前倾向于内皮细胞激活和损伤的一元化学说,其中肾脏损害导致的蛋白尿是评价PIH严重程度较客观的指标。中性粒细胞明胶酶相关脂质运载蛋白(NGAL)是一种新发现的脂质运载蛋白(lipocalin),已有研究证实,NGAL与急慢性  相似文献   

6.
目的:探讨人γ干扰素诱导蛋白16(IFI16)在子痫前期(PE)孕妇胎盘组织和血清中的表达及其与PE发病的相关性。方法:分别采用免疫组化法、实时荧光定量PCR技术和蛋白印迹法检测胎盘组织中IFI16表达;ELISA法检测血清IFI16及重组IFI16(r IFI16)处理后内皮细胞培养上清液中内皮素-1(ET-1)和可溶性血管内皮黏附分子(s VCAM-1)的浓度,分析PE孕妇血清IFI16水平与临床指标之间的相关性。结果:IFI16在PE组胎盘组织中的阳性表达率明显高于对照组(P0.05);与对照组相比,PE组胎盘组织中IFI16 mRNA和蛋白表达水平明显升高(P0.01);IFI16在PE组孕妇血清中的水平显著高于对照组(P0.01),且与孕妇收缩压(r=0.62,P0.001)、24h尿蛋白定量(r=0.723,P0.001)及相应胎盘组织中IFI16 mRNA表达水平(r=0.527,P0.05)呈正相关;r IFI16处理后,细胞培养上清液中ET-1和s VCAM-1浓度明显升高。结论:IFI16在PE孕妇胎盘组织和血清中的水平明显升高,并与内皮细胞损伤相关,提示IFI16可能通过损伤血管内皮细胞参与了PE的发病。  相似文献   

7.
目的通过对孕妇胎盘组织中解整合素金属蛋白酶10(a disintegrin and metalloproteinase 10,ADAM10)的检测,探讨ADAM10与子痫前期发病的关系。方法选择2009年9月至2012年3月在北京大学人民医院产科住院分娩的30例重度子痫前期(子痫前期组)和30例正常孕妇(正常妊娠组),采用反转录聚合酶链反应(RT—PCR)方法检测两组孕妇胎盘组织中ADAM10 mRNA的表达,并采用免疫组化二步法和蛋白质印迹法(Western Blot)检测胎盘组织中ADAM10蛋白的表达。结果ADAM10表达于胎盘组织的细胞滋养细胞和合体滋养细胞的细胞浆和细胞核中。子痫前期组中ADAM10 mRNA及蛋白的表达均明显高于正常妊娠组(P〈0.05)。结论重度子痫前期胎盘组织中ADAM10的过度表达可能与子痫前期的发生和发展有关。  相似文献   

8.
目的:研究PTEN在子痫前期胎盘组织及正常妊娠胎盘组织中的表达以探讨其与子痫前期发病的关系。方法:通过逆转录聚合酶链反应法检测37例重度子痫前期、22例轻度子痫前期及53例正常妊娠胎盘组织中PTEN的核酸表达水平,运用免疫组织化学检测PTEN在胎盘组织中的定位,通过免疫印迹法检测PTEN蛋白表达的水平。结果:免疫组织化学技术显示,PTEN选择性表达于胎盘血管内皮细胞浆中,RT-PCR及免疫印迹结果显示:重度子痫前期胎盘组织中PTEN的表达量低于轻度子痫前期及正常妊娠,差异有统计学意义(P<0.05)。结论:与正常妊娠及轻度子痫前期相比,重度子痫前期时PTEN表达发生改变,提示PTEN在重度子痫前期的发病机制中可能发挥了作用。  相似文献   

9.
目的:检测子痫前期孕妇胎盘组织及血清中干扰素-γ诱导蛋白10(IP-10)的表达情况,探讨其与子痫前期发病的关系。方法:收集正常妊娠、轻度子痫前期、重度子痫前期孕妇的胎盘组织及血清,采用ELISA、实时荧光定量PCR及Western blot方法检测IP-10在3组孕妇胎盘组织及血清中的表达变化。结果:ELISA结果显示,与正常对照组相比,轻度子痫前期组、重度子痫前期组孕妇血清中IP-10表达均明显增加(P均<0.05);实时荧光定量PCR及Western blot结果显示,与正常对照组相比,轻度子痫前期组、重度子痫前期组孕妇胎盘组织中IP-10 mRNA及蛋白表达水平均有不同程度增高(P均<0.05)。结论:子痫前期孕妇胎盘及血清中IP-10表达升高,可能与子痫前期的发病有关。  相似文献   

10.
目的:探讨中性粒细胞明胶酶相关脂质运载蛋白(NGAL)在妊娠期糖尿病(GDM)患者血清、脐血及胎盘组织中的表达及其与新生儿体重的相关性。方法:选取2017年6月至2017年11月于河北省人民医院产科行剖宫产术的GDM患者49例、正常妊娠(NGT组)孕妇39例。ELISA法测定母血、脐血血清NGAL水平,RT-PCR及Western blot法测定胎盘组织中NGAL mRNA及其蛋白表达。结果:GDM组母血、脐血血清NGAL水平均高于NGT组,胎盘组织中NGAL mRNA和蛋白表达量高于NGT组,两组比较差异有统计学意义(P0.01)。NGT组和GDM组孕妇血清NGAL水平与脐血均呈正相关(r=0.399,P=0.012;r=0.349,P=0.014);GDM组孕妇血清NGAL水平与胎盘组织NGAL mRNA(r=0.848,P=0.008)、蛋白(r=0.636,P=0.011)及新生儿体重(r=0.363,P=0.014)、胰岛素抵抗指数(r=0.312,P=0.044)均呈正相关。结论:GDM患者外周血NGAL水平的增加主要可能源于胎盘组织NGAL因子的过分泌,并通过增加胰岛素抵抗(IR)参与了GDM的发生。NGAL能通过胎盘转运至胎儿并进一步影响胎儿的宫内生长发育。  相似文献   

11.
目的:探讨子痫前期患者外周血及胎盘组织中半乳糖凝集素1(galectin-1,Gal-1)的表达及意义。方法:选取我院收治的早发型重度子痫前期患者53例为观察组,同期入院体检正常的孕妇53例为对照组。采用酶联免疫法检测血清Gal-1的浓度,经免疫组织化学法检测胎盘组织Gal-1蛋白的表达。结果:观察组和对照组外周血Gal-1浓度分别为(38.59±9.02)ng/L和(27.33±8.31)ng/L,2组比较差异有统计学意义(t=6.684,P<0.001)。观察组胎盘组织Gal-1的表达高于对照组,差异有统计学意义(Z=5.632,P<0.001)。结论:Gal-1可能与早发型重度子痫前期的发病有关,或可成为有价值的预测子痫前期的生物标记物。  相似文献   

12.
目的:探讨妊娠早期孕妇血清胎盘蛋白13(PP13)水平变化对早发型重度子痫前期(ESPE)的预测价值.方法:在妊娠10~13周采用全自动时间荧光免疫分辨技术检测7例ESPE患者和35例正常孕妇血清PP13水平.结果:血清PP13水平以中位数倍数(MoM)表示,ESPE孕妇血清PP13明显低于正常对照组(0.52 MoM vs 1.00 MoM,P<0.05).PP13水平以0.72MoM为切割值,曲线下面积为92.2%,早期预测ESPE的灵敏度为100%,特异度为77.1%.结论:妊娠早期血清PP13是预测ESPE的理想标志物.  相似文献   

13.
目的:探讨子癎前期患者及正常妊娠晚期妇女血清TPA、HCG的变化特点及临床意义。方法:将51例子癎前期患者设为实验组,分为轻度(A组)、重度(B组),33例正常晚孕者设为对照组,测定实验组、对照组TPA及HCG变化,并进行比较。结果:实验组TPA的浓度与对照组比较差异有显著性(P<0.05),实验B组与对照组比较差异有非常显著性(P<0.01),且与病情严重程度呈正相关;实验组HCG浓度与对照组比较差异有显著性(P<0.05)。实验A组与对照组比较差异非常显著(P<0.01)。结论:子癎前期患者外周血TPA增高与滋养细胞凋亡增加有关,而HCG分泌增加与缺氧状态下滋养细胞反应性增生有关,提示子癎前期患者有明显的滋养细胞增生与分化异常存在。TPA作为外周血滋养细胞凋亡的标志物,可间接反映胎盘功能的变化。  相似文献   

14.
We investigated the global placental gene expression profile in severe preeclampsia. Twenty-one women were randomly selected from 50 participants with uncomplicated pregnancies to match 21 patients with severe preeclampsia. A 30 K Human Genome Survey Microarray v.2.0 (Applied Biosystems) was used to evaluate the gene expression profile. After RNA isolation, five preeclamptic placentas were excluded due to poor RNA quality. The series composed of 37 hybridizations in a one-channel detection system of chemiluminescence emitted by the microarrays. An empirical Bayes analysis was applied to find differentially expressed genes. In preeclamptic placentas 213 genes were significantly (fold-change  2 and p  0.01) up-regulated and 82 were down-regulated, compared with normal placentas. Leptin (40 fold), laeverin (10 fold), different isoforms of β-hCG (3–6 fold), endoglin (4 fold), FLT1 (3 fold) and FLT4 (2 fold) were up-regulated. PDGFD was down-regulated (2 fold). Several differentially expressed genes were associated with Alzheimer disease, angiogenesis, Notch-, TGFβ- and VEGF-signalling pathways. Sixteen genes best discriminated preeclamptic from normal placentas. Comparison between early- (<34 weeks) and late-onset preeclampsia showed 168 differentially expressed genes with oxidative stress, inflammation, and endothelin signalling pathways mainly involved in early-onset disease. Validation of the microarray results was performed by RT-PCR, quantitative urine hCG measurement and placental histopathologic examination. In summary, placental gene expression is altered in preeclampsia and we provide a comprehensive list of the differentially expressed genes. Placental gene expression is different between early- and late-onset preeclampsia, suggesting differences in pathophysiology.  相似文献   

15.
目的:探讨脂蛋白脂酶(LPL)在重度子痫前期产妇血清和胎盘组织中的表达及意义。方法:收集2008年9月至2009年5月在上海市第六人民医院产科住院并分娩的重度子痫前期产妇26例为子痫前期组,选择同期分娩的正常产妇30例为对照组。用酶法检测血脂浓度,ELISA法检测血清LPL浓度,RT-PCR法和Western blot法检测胎盘组织LPL基因和蛋白的表达。结果:①子痫前期组血脂浓度明显高于对照组(P<0.05)。②子痫前期组血清LPL浓度及胎盘组织LPL基因和蛋白表达水平均明显低于对照组(P<0.05)。③子痫前期组血清LPL浓度与胎盘组织LPL蛋白表达水平呈正相关(r=0.421,P<0.05),与甘油三酯(TG)呈负相关(r=-0.668,P<0.01),与高密度脂蛋白(HDL)呈正相关(r=0.876,P<0.01)。结论:子痫前期患者机体脂蛋白脂酶表达降低,脂蛋白脂酶可能通过参与高血脂代谢在子痫前期发病过程中起着重要作用。  相似文献   

16.
Dysferlin (DYSF) and myoferlin (MYOF), members of the ferlin family of membrane proteins, are co-expressed in human placental syncytiotrophoblast (STB). Although the role of these ferlin proteins in the placenta has yet to be established, it has been suggested that DYSF and MYOF may contribute to the stability of the apical STB plasma membrane. The release of STB-derived cellular debris increases in the setting of preeclampsia (PE), suggesting relative destabilization of the hemochorial interface. To test whether PE was associated with alterations in placental expression of DYSF and/or MYOF, a cross-sectional study was performed using specimens of villous placenta collected form women with severe PE (n = 10) and normotensive controls (n = 10). DYSF and MYOF expression were examined using quantitative real–time RT-PCR, immunoblotting, and immunofluorescence labeling of tissue specimens. Placental DYSF expression was 57% lower at the mRNA level (p = 0.03) and 38% lower at the protein level (p = 0.026) in severe PE as compared to normotensive subjects. There were no differences in placental MYOF protein or mRNA expression between these groups. No appreciable changes in the distribution of DYSF or MYOF within placental villi was observed in PE relative to control specimens. We conclude that DYSF expression is reduced in severe PE relative to gestational age-matched controls. As DYSF has a role in membrane repair, these data suggest a role for DYSF in the stability of the apical STB plasma membrane and may account, at least in part, for the increased shedding of microparticles from this membrane in PE.  相似文献   

17.
Objective. Human placental growth hormone (hPGH) is produced by human placenta and plays a central role in the maternal metabolic adjustments to pregnancy. The objective of this study was to investigate the maternal serum concentration of hPGH at 11–13 weeks of gestation in pregnancies that subsequently developed preeclampsia (PE), and to examine the possible association with uterine artery pulsatility index (PI) and maternal serum pregnancy-associated plasma protein-A (PAPP-A). Methods. The maternal serum concentration of hPGH at 11–13 weeks was measured in a case–control study from 60 cases that developed PE and 120 unaffected controls. The measured hPGH concentration was converted into a multiple of the expected median (MoM) in unaffected pregnancies. Regression analysis was used to determine the significance of association between hPGH MoM with uterine artery PI MoM and PAPP-A MoM. Results. In the pregnancies that subsequently developed PE the median serum hPGH concentration was not significantly different from that in the unaffected group (0.92 versus 1.00 MoM), whereas uterine artery PI was increased (1.31 versus 1.01 MoM) and serum PAPP-A was decreased (0.76 versus 1.01 MoM). In the group that developed PE there was no significant association between serum hPGH MoM and gestational age at delivery, uterine artery PI MoM, or serum PAPP-A MoM. Conclusion. The finding that in the PE group serum hPGH level during the first trimester is normal suggests that it is unlikely that this hormone plays a role in the pathogenesis of PE.  相似文献   

18.
Background. Total or cellular fibronectin (FN) determinations have been used to differentiate between normal and preeclamptic pregnants. The purpose of this study was to examine the relationship between maternal serum FN levels and the extracellular matrix molecule contents of placental tissue, such as FN, hyaluronic acid (HA) and hydroxyproline (HP) levels. Material and Methods. We obtained maternal blood samples and placental tissue samples from healthy (n = 17, controls) and preeclamptic pregnants (n = 29). We also obtained cord blood samples for FN and HA determination from the same patients. FN and HA concentrations in the placenta and maternal and cord blood were measured by and enzyme-linked immunosorbent assay and HP contents in the placenta were measured by a colorimetric assay. Results. FN levels in maternal serum, cord blood, and placenta were significantly higher in preeclamptics than in controls (p<0.001, p<0.001 and p<0.05, respectively). HA concentrations in the cord blood and placenta were found to be elevated in preeclamptics (p<0.05 and p<0.01). Preeclamptics had significantly higher placental HP levels than controls (p<0.001). Similar statistically significant results were obtained when the pregnant subjects classified as nulliparous and multiparous. There was no difference in ECM molecule levels between nulliporous and multiparous women in preeclamptic pregnant group. In regression analysis maternal serum FN levels were correlated with placental HA and HP levels (p<0.01 and p<0.01). There was a positive correlation between cord blood FN and both placental HP (p<001) and HA levels (p<0.01). FN levels in maternal serum, cord blood, and placenta were also negative correlated with fetal birth weight (p<0.01, p<0.05 and p<0.05, respectively). Conclusion. FN in maternal serum, cord blood, and placenta is increased with elevated placental HA and HP levels, probably reflecting placental basement membrane alterations during preeclampsia.  相似文献   

19.
Objective. The aim of this study was to evaluate serum resistin levels in women with preeclampsia compared to those in normal pregnant women and normal non-pregnant women, and to examine placental resistin expression. Methods. Serum resistin levels were measured by enzyme-linked immunosorbent assay and placental resistin expression was determined by immunohistochemistry. Results. Serum resistin levels were significantly elevated in women with preeclampsia compared to normal pregnant women and non-pregnant women. There was no significant difference in placental resistin expression. Conclusion. The placenta may not be the origin of the resistin that contributes to increased serum levels in women with preeclampsia.  相似文献   

20.
目的:研究RECK和MMP-9在不同子宫内膜组织中的表达,探讨两者在子宫内膜癌的发生、发展和浸润转移中的作用。方法:应用链霉菌抗生物素蛋白-过氧化酶(SP)免疫组化法检测42例子宫内膜癌组织、15例子宫内膜不典型增生组织及26例正常增生期子宫内膜组织中RECK蛋白及MMP-9蛋白表达情况。结果:与正常增生期子宫内膜组织及子宫内膜不典型增生组织相比,子宫内膜癌组织中RECK蛋白阳性表达率显著降低(χ2=9.307,P<0.05),MMP-9蛋白阳性表达率显著增高(χ2=11.438,P<0.05),RECK蛋白与MMP-9蛋白在子宫内膜癌中的表达存在明显负相关(P<0.01)。RECK蛋白的表达水平与临床分期、组织学分级、肌层浸润深度及淋巴结转移密切相关(均P<0.05);MMP-9蛋白的表达水平与临床分期、组织学分级、肌层浸润深度密切相关(均P<0.05),而与淋巴结转移无关。结论:RECK蛋白的表达缺失和MMP-9的表达可能与子宫内膜癌的发生、发展及浸润转移有关。  相似文献   

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