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ID:31957841
大小:2.95 MB
页数:42页
时间:2019-01-29
《半乳糖凝集素-1在子痫前期的表达与意义》由会员上传分享,免费在线阅读,更多相关内容在应用文档-天天文库。
1、中文摘要13.0统计软件分析数据。结果:1子痫前期组(早发型组+晚发型组)外周血血清中Gal一1水平(34.48士7.02)pg/ml与对照组(28.964-9.36)pg/ml比较,差异有统计学意义(氏O.05);早发型组Gal一1水平(37.22+6.44)pg/ml明显高于晚发型组(31.75-4-7.59)pg/ml,差异有统计学意义(氏0.01);晚发型中SPE组Gal.1水平(35.22士6.40)pg/ml明显高于MPE组(28.80+7.37)pg/ml,差异有统计学意义(火0.05)。2子痫前期组(早发型组+晚发型组)胎盘组织中Gal.1的表达(1.73-4-0.7
2、6)与对照组(1.05如.71)比较,差异有统计学意义(火0.05);早发型组Gal.1表达(1.93-4-0.68)高于晚发型组(1.54-4-0.82),差异有统计学意义(氏0.05);晚发型中SPE组Gal.1表达(1.95-4-0.89)明显高于MPE组(1.19-4-0.57),差异有统计学意义(氏0.05)。3晚发型组、早发型组、对照组外周血血清Gal—l浓度与胎盘Gal一1表达均呈正相关性(F0.555,f0.367,r=0.375,均P<0.05)。4早发型与晚发型组血清Gal.1浓度与24小时尿蛋白、分娩前收缩压、舒张压呈正相关,差异有统计学意义(火o.05);正常
3、妊娠组血清Gal一1浓度与临床指标无关(胗0.05)。5Gal.1在对照组、子痫前期组胎盘滋养细胞,绒毛毛细血管内皮细胞和基质细胞表达均呈阳性,在绒毛间质表达呈弱阳性。子痫前期胎盘上Gal.1的表达较对照组明显升高,Gal.1在早发型子痫前期组表达最强,与晚发型组有明显差异,晚发组中SPE组表达强于MPE组。结论:1子痫前期孕妇血清和胎盘中Gal—l水平明显升高,提示Gal.1参与子痫前期的发病过程。2子痫前期血清Gal.1浓度与24小时尿蛋白、分娩前收缩压、舒张压呈正相关,考虑Gal.1与子痫前期的严重程度相关。3子痫前期孕妇血清Gal一1与胎盘中Gal一1呈正相关,提示Gal一1
4、参与了子痫前期中胎盘功能损伤的发病机制。关键词:子痫前期;半乳糖凝集素.1;免疫耐受;细胞凋亡;滋养细胞英文摘要Expressionandsignificanceofgalectin·1inthepreeclampsiaPreeclampsia(PE)isthemultiplesystemdiseaseduringpregnancywithhypertension,proteinuriaasthemaincharacteristics,andofteninvolvedcriticalorganssuchascardiovascular,kidneys,liverandplacenta
5、.Maternalandchildrenhealthareaffectedseriouslybypreeclampsia,whichisthekeyreasonfortheincreasingmatemalandperinatalmortality.Sofar,itspathogenesisisnotelucidatedclearly.Someresearchershaveproposedinthepathogenesisofpreeclampsiaisduetouterinespiralartery订ophoblasficrecastdisorders,leadingtoplace
6、ntalischemiaandhypoxia,andthereleaseofavarietyofplacentalfactorsintothem.aternalbloodcirculationandpromotetheactivationofsystemicinflammationandendothelialdamage,therebycausingavarietyofclinicalsymptomsofpreeclampsiaandeclampsia.Galectin—l(Gal-1)isamultifunctionalregulatorinvolvedinavarietyofph
7、ysiologicalandpathologicalprocessesofcelladhesion,proliferation,apoptoticandinflammatoryreactions.Gal一1expressedintheplacentaofmaternal-fetalinterfacesyncytiotrophoblastandimmunecells,mediatedmaternal—fetalinterfaceThl/Th2shifttow
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