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ID:33005615
大小:1.57 MB
页数:40页
时间:2019-02-19
《叶酸缺乏通过线粒体途径抑制孕鼠子宫内膜蜕膜细胞凋亡》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、重庆医科大学硕士研究生学位论文FOLATEDEFICIENCYDECREASESAPOPTOSISOFENDOMETRIUMDECIDUALCELLSINPREGNANTMICEVIATHEMITOCHONDRIALPATHWAYABSTRACTObjective:Itiswellknownthatmaternalfolatedeficiencyresultsinadversepregnancyoutcomes,includingembryonicmalformations,abortion,preterm,lowbirthweightandsoon.Amongthem,therelation
2、shipbetweenfolatedeficiencyandneuraltubedefects(NTD)hasbeenrecognizedbythescholars.Previousstudiesfocusedtheireyesontheeffectoffolatedeficiencyonthefetuswhileignoringitsimpactonthematernalaspects.Inadditiontoaspectsinembryonicdevelopment,maternaluterinereceptivityanddecidualizationofstromalcellsarea
3、lsoveryimportantforasuccessfulpregnancy.Ourpreviousstudyrevealedthattherewasnoeffectoffolatedeficiencyonembryoimplantation,andboththeexpressionofuterinereceptivitymarkergenesandthenumberofimplantationsitesshowednosignificantdifferencebetweenthefolatedeficiencygroupandcontrolgroup.However,theoutcomeo
4、fthefolate-deficientpregnantmicewasnotfavorable,whichindicatesmoreembryolossandsmallerembryovolume.Inthisstudy,weinvestigatedwhetherapoptosisofthedecidualcellswasimpairedunderfolate-deficientconditionsandexploredmaternaluterine4万方数据重庆医科大学硕士研究生学位论文endometriumdecidualizationinthatcondition.Methods:Afo
5、late-deficientpregnantmousemodelandanormaldietpregnantmicemodelwereestablished.Flowcytometry,JC-1detectionandTUNELwereusedtodetectapoptosisofthedecidualcellsisolatedfrompregnantmiceonday7and8.TEMwasusedtoobservethemorphologyofmitochondriaandendoplasmicreticulum.Immunohistochemistrywasusedtodetectthe
6、proteinexpressionandlocationofBaxandBcl2.TheexpressionofBax、Bcl2、cleaved-Caspase3、pro-Caspase3、cytochromecweredetectedusingWesternblot.Immunofluorescenceandlaserscanningconfocalmicroscopewereusedtoobservethereleaseofcytochromecfrommitochondriatocytoplasm.WesternblotandRT-PCRwereusedtodetecttheexpres
7、sionofgenesHoxa10,BMP2,MMP2,MMP9,whichwererelatedtoendometriumdecidualization.Results:Decidualcellsofmiceinthecontrolgroupexhibiteddilationoftheendoplasmicreticulumanddistendedmitochondria,whilethefol
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