简介：现在的学习被设计在N1E-115房间和内在的机制在神经突生长上调查橡黄素的角色。橡黄素被显微镜学，长矛(tm)营地384工具包，和西方的污点分析的使用在vitro在N1E-115房间在神经突，神经突长度，细胞内部的营地内容，和Gap-43表示的房间数字上为它的效果评估分别地。我们的结果证明橡黄素能以一种集中依赖者方式增加神经突长度，但是没在房间的数字上有效果。橡黄素显著地在一个时间依赖者和集中依赖者举止增加了细胞的营地的表示。Gap-43表示以一种时间依赖者方式是起来调整的。在结论，橡黄素能通过增加细胞内部的营地水平和Gap-43表示支持神经突生长。

简介：Benignprostatichyperplasia(BPH)isanage-relateddiseaseofunknownetiology,characterizedbyprostaticenlargementcoincidentwithdistinctalterationsintissuehistology.Inthepresentstudy,weinvestigatedwhethertriptolidecanpreventtestosterone-inducedprostatichyperplasiainrats.Castrationwasperformedviathescrotalrouteafterurethaneaesthesia.BPHwasinducedinexperimentalgroupsbydailysubcutaneousinjectionsoftestosteronepropionate(TP)fortwoweeks.Triptolidewasadministereddailybyoralgavageatadoseof100and50μg×kg~(-1)for2weeks,alongwiththeTPinjections.Onday14,theanimalswerehumanelykilledbycervicaldislocationafteraesthesia.Prostateswereexcised,weighed,andusedforhistologicalstudies.Testosteroneanddihydrotestosterone(DHT)levelsinserumandprostateweremeasured.Theresultsshowedthattriptolidesignificantlyreducedtheprostateweight,andthetestosteroneandDHTlevelsinboththeserumandprostate.HistopathologicalexaminationalsoshowedthattriptolidetreatmentsuppressedTP-inducedprostatichyperplasia.Inconclusion,triptolideeffectivelyinhibitsthedevelopmentofBPHinducedbytestosteroneinaratmodel.