DHEAisanimportantsourceofandrogens,andisaneffectiveantiapoptoticfactor.

Androgenreceptor^[1]

DHEAisaneffectiveantiapoptoticfactor,reversingtheserumdeprivation-inducedapoptosisinprostatecancercells(DU145andLNCaPcelllines)aswellasincoloncancercells(Caco2cellline).DHEAsignificantlyreducesserumdeprivation-inducedapoptosisinall3cancercelltypes,quantitatedwiththeAPOPercentageassay(apoptosisisreducedfrom0.587±0.053to0.142±0.0016or0.059±0.002aftertreatmentfor12hourswithDHEAorNGF,respectively;n=3,P<0.01), and="" by="" flow="" cytometry="" analysis="" (facs)="" for="" du145="" cells.="" the="" antiapoptotic="" effect="" of="" dhea="" is="" dose="" dependent="" with="" an="" ec50="" at="" nanomolar="" concentrations="">₅₀:11.2±3.6nMand12.4±2.2nMinDU145andCaco2cells,respectively)^[1].DHEAistheprincipalsexsteroidprecursorinhumansandcanbeconverteddirectlytoandrogens.DHEA(≥1μM)causesadose-dependentinhibitionofChub-S7proliferation,asassessedbythymidineincorporationassays.DHEAtreatmentinhibitsexpressionofthekeyglucocorticoid-regulatinggenesH6PDH(≥100nM)andHSD11B1(≥1μM)indifferentiatingpreADIpocytesinadose-dependentmanner.Inkeepingwiththisfinding,DHEAtreatment(≥1μM)resultsinamarkedreductionin11β-HSD1oxoreductaseactivity(≥1μM)andaconcurrentincreaseindehydrogenaseactivityatthehighestDHEAdoseused(25μMDHEA)indifferentiatedadipocytes^[2].

DHEAinthediet(0.45%w/w)ofmaleB6mice(groupsoffivemice)treatedfor8weeksledtosignificantdecreasesinbodytemperaturecomparedwithmicefedthecontrolAIN-76Adiet.Asimilarcomparisonindicatedthatcontrolandpair-fedmicearealsosignificantlydifferent.AnimalsfedDHEAhavesignificantlylowertemperaturesthanmicefedthecontroldiet26/29timestested;micepairfedtothoseontheDHEAdietarelessaffected,with8/29valuessignificantlylowerthaninmicefedAIN-76Aadlibitum.ThetemperaturesofmicefedDHEAorpairfedtoDHEAaresignificantlydifferent21/29timestested.BodyweightsaresignificantlygreaterinmicefedthecontroldietthaninmicefedDHEAorpairfedtoDHEA.Foodintake(gramsperday)fromcagesareaveragedforeachweek(n=7),exceptforWeek9(n=3).TheamountoffoodintakeissignificantlydecreasedinmicefedDHEA.Bydesign,micepairfedtoDHEAateaboutthesameamount.Thus,itappearsthatDHEAreducesbodytemperaturebyfoodrestrictionandbyaseparatemechanism^[3].

• [1].AnagnostopoulouV,etal.Differentialeffectsofdehydroepiandrosteroneandtestosteroneinprostateandcoloncancercellapoptosis:theroleofnervegrowthfactor(NGF)receptors.Endocrinology.2013Jul;154(7):2446-56.

  [2].McNelisJC,etal.Dehydroepiandrosteroneexertsanti-glucocorticoidactiononhumanpreadipocyteproliferation,differentiationandglucoseuptake.AmJPhysiolEndocrinolMetab.2013Nov1;305(9):E1134-44.

  [3].CatalinaF,etal.Decreaseofcorebodytemperatureinmicebydehydroepiandrosterone.ExpBiolMed(Maywood).2002Jun;227(6):382-8.

Chub-S7cellsareincubatedinDMEMcontainingcoldDHEA(20nM)andtritiatedDHEA(0.2μCi/well)for48h.Followingincubation,steroidsareextractedusingdichloromethaneseparatedbythin-layerchromatographyusingn-hexane/1-hexanol(75:25)asthemobilephasesystem.MetabolitesareidentifiedbycomigrationwithunlabeledreferencesteroidsthatarevisualizedbyexposuretoLieberman-Burchardreagent(ethanol-aceticanhydride-sulfuricacid).SteroidconversionisquantifiedusingaLabLogicAR-200scanner.Proteinconcentrationismeasuredusingacolorimetric96-wellplateassayandusedtonormalizeconversion.Activityisexpressedaspercentconversion^[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

DHEAisdissolvedinDMSOandstored,andthendilutedwithappropriatemediumbeforeuse^[2].

Chub-S7preadipocytesandhumanprimarypreadipocytesareseededintoa24-wellplateatdensities1×10⁵and2.5×10⁵respectively.Followingovernightculture,mediumissupplementedwithDHEA,androstenediol,orDHEAS(0-100μM).Following24-,48-,or72hincubation,cellproliferationisassessedbyincubationwithradiolabeledthymidine(0.2μCi/well)forthefinal6hofculture.ProteinsareprecipitatedwithTCA,andcellsarescrapedinNaOH.Therespectivecontentofradiolabelednuclearmaterialintheresultinglysatesisanalyzedbyscintillationcounting.Dataareexpressedaspercentageofcontrol^[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

DHEAispreparedin0.9%NaCl(Mice)^[3].

Mice^[3]
MicearefedPurinaLabChowuntilthestartofexperiments(Day0).GroupsoffivemicearethenfedpelletedAIN-76AdietcontainingeithernoadditiveorDHEA(0.45%w/w)between0900and1000hr.Dietsarestoredat4°Cfornolongerthansixmonthstomaintainoptimalactivity.Micearegiventhedietsadlibitum,exceptformicethatarepairfedtomicetreatedwithDHEA.TheamountsofAIN-76Adietthepair-fedmicereceivedaredeterminedbytheweightoffoodconsumedbytheDHEA-fedmiceonadailybasis.Bodyweights(grams)aremeasuredatdifferenttimepointsstartingatDay1andendingatDay59.Dailyfoodintakes(gramsperday)aredeterminedbyweighingthefoodconsumedpercageoffivemice.Themean±SEMvaluesarecalculatedforweeks1to8(n=7);week9hadonly3days.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

• [1].AnagnostopoulouV,etal.Differentialeffectsofdehydroepiandrosteroneandtestosteroneinprostateandcoloncancercellapoptosis:theroleofnervegrowthfactor(NGF)receptors.Endocrinology.2013Jul;154(7):2446-56.

  [2].McNelisJC,etal.Dehydroepiandrosteroneexertsanti-glucocorticoidactiononhumanpreadipocyteproliferation,differentiationandglucoseuptake.AmJPhysiolEndocrinolMetab.2013Nov1;305(9):E1134-44.

  [3].CatalinaF,etal.Decreaseofcorebodytemperatureinmicebydehydroepiandrosterone.ExpBiolMed(Maywood).2002Jun;227(6):382-8.

288.42

C₁₉H₂₈O₂

53-43-0

RoomtemperatureincontinentalUS;mayvaryelsewhere

10mMinDMSO

*"<1 mg/ml"="" means="" slightly="" soluble="" or="" insoluble.="" "≥"="" means="" soluble,="" but="" saturation="">

Purity:>98.0%

SelectBatch:HY-14650-09520HY-14650-09991

DataSheet(136KB)SDS(389KB)

COA(94KB)HNMR(176KB)

HandlingInstructions(1252KB)

• [1].AnagnostopoulouV,etal.Differentialeffectsofdehydroepiandrosteroneandtestosteroneinprostateandcoloncancercellapoptosis:theroleofnervegrowthfactor(NGF)receptors.Endocrinology.2013Jul;154(7):2446-56.

  [2].McNelisJC,etal.Dehydroepiandrosteroneexertsanti-glucocorticoidactiononhumanpreadipocyteproliferation,differentiationandglucoseuptake.AmJPhysiolEndocrinolMetab.2013Nov1;305(9):E1134-44.

  [3].CatalinaF,etal.Decreaseofcorebodytemperatureinmicebydehydroepiandrosterone.ExpBiolMed(Maywood).2002Jun;227(6):382-8.

他替瑞林口服促甲状腺素释放激素他替瑞林CAS号:103300-74-9英文名称:Taltirelin英文同义词:TA0910;Taltirelin;Taltireline;Ceredist,TA-0910;TaltirelinAcetate;TA-0910,taltirelin;TaltirelininterMediate;TALTIRELININTERMEDIATES;TaltirelinAcetate,TA-0910;L-Prolinamide,(4S)-hexahydro-1-methyl-中文名称:他替瑞林中文同义词:他替瑞林;醋酸他替瑞林;1-METHYL-4,5-DIHYDROOROTYL-HIS-PRO-NH2;(4S)-N-[(2S)-1-[(2S)-2-氨基甲酰基吡咯烷-1-基]-3-(3H-咪唑-4-基)-1-氧代丙-2-基]-1-甲基-2,6-二氧代-1,3-二氮杂己环-4-甲酰胺CBNumber:CB31177191分子式:C17H23N7O5分子量:405.41MOLFile:103300-74-9.mol化学性质安全信息用途供应商86化学性质安全信息用途供应商86他替瑞林化学性质熔点:72-75°比旋光度:25D-13.6°(c=1inwater)密度:1.447±0.06g/cm3(Predicted)储存条件:Storeat+4°C酸度系数(pKa):9.32±0.40(Predicted)安全信息他替瑞林性质、用途与生产工艺口服促甲状腺素释Chemicalbook放激素他替瑞林是一种垂体激素释放兴奋药，由日本田边三菱制药株式会社研制成功，商品名Taltirelin，属于化药新药3.1类，目前临床用于改善脊髓小脑变性患者的运动失调最为有效的药物。他替瑞林（Taltirelin）是世界上第一个批准的口服促甲状腺素释放激素(TRH)，除具有内分泌作用外，还可发挥一定的中枢神经系统(CNS)作用，包括提高运动活性，拮抗利舍平诱导的体温降低，以及拮抗戊巴比妥诱导的睡眠。该品种由日本田边三菱制药株式会社开发，2000年9月首次在日本上市，用于改善脊髓小脑变性病人的共济失调。脊髓小脑共济失调(SCAs)旧称常染色体显性共济失调，是一组以共济失调、辨距不良为主要临床表现的中枢神经系统慢性变性疾病。2000年9月前，促甲状腺素释放激素（TRH）注射液是唯一用于治疗该类疾病的药物。他替瑞林是TRH的结构修饰改造药物，药理学研究显示本品经由脑TRH受体对CNS产生强而持久的多重作用。本品对CNS的兴奋作用比TRH强10～100倍，作用持续时间比TRH长约8倍。本品对TRH受体的亲和力约为TRH的1/11，因而本品的内分泌作用比TRH弱，但本品在体内比TRH稳定。另外本品对促甲状腺素(TSH)释放的作用为TRH的1/6-1/11，TSH释放是由一个包括甲状腺激素的强负反馈系统调节的，对中枢神经系统具有较强的作用，但同时其激素样作用较小，因此副作用较少。不良反应主要是消化系统反应，包括呕吐、恶心和胃不适。所有的不良反应均为轻中度，在治疗期间及(或)停药后消失。

• 

  资质认证

  获得国家资质，权威认证！

• 

  全国联保

  全国联保，官方无忧售后

• 

  正规发票

  正规发票，放心购买

• 

  签订合同

  签订合同，保障您的权益

购物指南

购物流程

注册登录

账户管理

订单查看

常见问题

FAQS

蚁豆兑换

物流说明

评论规则

发票说明

价格说明

支付说明

服务协议

版权声明

诚信保障

免责申明

销售协议

隐私条款

法律申明

售后服务

退换货政策

工作时间

退款说明

售后支持

售后申请表模板列表

关于我们

公司简介

联系我们

资质证书

人才招聘

商务合作

万众创业

网址导航

蚂蚁淘商城

科研狗

苏州蚂蚁淘

生物信息网

现货促销

微信公众号

Chemicell中国 | 转染试剂24765 | percipiobio价格 | Probetex价格 | bioroute华东代理 | Glixx Laboratories厂家 | Sigma代理 | 蚂蚁淘 | 染色体倍性分析仪

copyright©2005-2021 蚂蚁淘在线版权所有　苏州蚂蚁淘生物科技有限公司 www.assay-online.com ICP号：苏ICP备17049038号-16

/**/