慢性应激对卵泡发育的影响及自分泌 旁分泌调控机制研究-study on the influence of chronic stress on follicular development and the mechanism of autocrine paracrine regulation.docxVIP

结论：慢性应激可以影响小鼠的动情周期，影响小鼠卵泡的发育及排卵。外源性补充促性腺激素后，慢性应激组排卵数明显减少，HE染色结果显示：慢性应激增加了卵泡的闭锁，干扰了卵泡的发育和排卵，即使外源性给予促性腺激素仍不能使早期卵泡发育和排卵恢复正常，提示非促性腺激素类因素参与慢性应激干扰卵泡发育和排卵。RT-PCR结果显示，慢性应激后，相比正常对照组，自分泌、旁分泌因子GDF-9、BMP-15表达水平有明显降低（P0.05），SCF、bFGF表达无明显变化。提示慢性应激通过下调卵源性的局部旁分泌因子GDF-9、BMP-15参与影响卵泡的发育。关键词：慢性应激；自分泌、旁分泌因子；卵泡；发育TheeffectofChronicstressonfolliculardevelopmentandmechanismofautocrine,paracrineregulatoryfactorsAbstractObjectiveObservetheeffectsofchronicstressonfolliculargrowthandtheestrousandtheeffectonthefollicledevelopmentofnon-gonadotropin-dependented.Thencheckoutfourparacrine-autocrinefactorsforRT-PCR,andseeiftheyparticipateintheprocessofchronicstressonfolliculargrowthandthedevelopmentofadisincentiveeffect.MethodsThroughtheestablishmentofchronicstressmodelinmice,andprepareHEsectionstoobservetheimpactionofthegrowthanddevelopmentofovarianfollicles.Fromthefirstdayofchronicstress(toexecuteended),micewerevaginaldischargeforsmear,Wrightstraintoobservethelineofestrouscycle.Addedbyexogenousgonadotropintoobservetheireffectionofrecoveryonovulationafterchronicstress.Usingreal-timePCRsemi-quantitativeexperimentaltodeterminetheself-secretedparacrinefactorswhichwereselected.Results(1)Chronicstressextendanddisorderthesexualcycleofmice.(2)ChronicstressInhibitefolliclematurationandovulationoccurringAddedexogenousgonadotropincannotmakethefolliculardevelopmentandovulationbacktonormalcompletely.Inthecourseofchronicstress,thesecretionofparacrinefactorGDF-9、BMP-15fromoocytemakeaevidencereductioninthelevelofmRNAandSCF、bFGFfromgranulosacellsdidnotchange.ConclusionChronicstresscanaffecttheestrouscycleinmice,affectingmousefollicledevelopmentandovulation.Addedexogenousgonadotropin,thechronicstressgroupsignificantlyreducedthenumberofovulation,HEstainingshowed:Chronicstressincreasedfollicleatresia,interfereswithfolliculardevelopmentandovulation,evenifaddexogenousgonadotropinstillcannotmaketheearlyfolliculardevelopmentandovulationbacktonormal,suggestingthatthenon-gonadotropin-classfactorsareinvolvedinchronicstress