Estradiolisahumansexhormoneandsteroid,andtheprimaryfemalesexhormone.

EstradiolinducesnewdendriticspinesandsynapsesonhippocampalCA1pyramidalcells.Estradioltreatmentresultedina46%increaseinNMDAreceptorbinding.EstradioltreatmentincreasesNMDAreceptorbindinginparallelwithdendriticspineandsynapsedensity.EstradioltreatmentresultsinincreasedsensitivityofCA1pyramidalcellstoNMDAreceptor-mediatedsynapticinputandthatthisincreaseiswellcorrelatedwiththeestradiol-inducedincreaseindendriticspinedensityintheapicaldendritictreeofthesecells^[1].EstradiolisfoundtoreduceBa²⁺entryreversIBLyviaCa²⁺channelsinacutelydissociatedandculturedneostriatalneurons.EstradiolalsoreducesBa²⁺currentsbutissignificantlylesseffectivethanEstradiolinratneostriatalneurons^[2]. Estradiolexertsadose-dependentinhibitionofIL-1-,TNF-,andIL-1andTNF-inducedproductionofbioassayableIL-6.EstradiolinhibitsbothTNF-inducedIL-6productionandosteoclastdevelopmentinprimarybonecellculturesderivedfromneonatalmurinecalvaria^[3].

Estradiolmediatesfluctuationinhippocampalsynapsedensityduringtheestrouscycleintheadultrat^[4].Estradiolalonecanreversetheovariectomy-induceddecreaseinspinedensity.EstradiolcombinedwithProgesteroneinitiallyincreasesspinedensityforaperiodof2to6hoursbutthenresultsinamuchsharperdecreasethanisobservedfollowingestradiolalone^[5]. 

• [1].WoolleyCS,etal.EstradiolincreasesthesensitivityofhippocampalCA1pyramidalcellstoNMDAreceptor-mediatedsynapticinput:correlationwithdendriticspinedensity.JNeurosci.1997Mar1;17(5):1848-59.

  [2].MermelsteinPG,etal.Estradiolreducescalciumcurrentsinratneostriatalneuronsviaamembranereceptor.JNeurosci.1996Jan15;16(2):595-604.

  [3].GirasoleG,etal.17beta-estradiolinhibitsinterleukin-6productionbybonemarrow-derivedstromalcellsandosteoblastsinvitro:apotentialmechanismfortheantiosteoporoticeffectofestrogens.JClinInvest.1992Mar;89(3):883-91.

  [4].WoolleyCS,etal.Estradiolmediatesfluctuationinhippocampalsynapsedensityduringtheestrouscycleintheadultrat.JNeurosci.1992Jul;12(7):2549-54.

  [5].WoolleyCS,etal.Rolesofestradiolandprogesteroneinregulationofhippocampaldendriticspinedensityduringtheestrouscycleintherat.JCompNeurol.1993Oct8;336(2):293-306.

Estradiolisdissolvedin0.01%ethanol.

Briefly,B9cells(5×10³/wellofa96-wellplate)areculturedwithaseriesofdilutionsofthesupernatantsinafinalvolumeof100mLofRPMI1640,supplementedwith5×10^-5mol/Lof2-mercaptoethanol,10%FBS,100U/mLpenicillin,and100μg/mLstreptomycininflat-bottommicrotiterplates.After42h,0.5μCiof[³H]thymidineisadded.6hlater,thecellsareharvestedandtheradioactivityincorporatedisdetermined.IL-6isquantitatedfromastandardcurvesetupwithknownamountsofrecombinanthumanormouseIL-6.Theanti-IL-6monoclonalantibodycompletelyinhibitedtheABIlityoftheB9cellstoproliferateinresponsetorecombinantmouseIL-6.Inaddition,wedeterminedthatB9cellsdonotproliferateinresponsetoIL-IorTNF,andthatantibodiestothesetwocytokinesdidnotaffectthecellproliferationinresponsetoIL-6.Further,itisestablishedthatneitherEstradiol(17β-estradiol),northe0.01%ethanolusedasvehicleintheseexperiments,hasanyeffectonthebioassay.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

Estradiolisformulatedinsesameoil.

AdultfemaleSpragueDawleyratsarehousedona12hrlight/darkcyclewithunlimitedaccesstofoodandwater.Theseanimalsareleftgonadallyintact(intact),ovariectomizedandtreatedwithestradiolbenzoate(OVX+E),orovariectomizedandtreatedwithsesameoilvehicle(OVX+O).ThehormonetreatmentregimenthatisusedintheseexperimentshasbeenshownpreviouslytoresultindifferencesinCA1pyramidalcelldendriticspineandsynapsedensity.Sixdaysbeforeelectrophysiologicalanalysis,animalsareovariectomizedunderMetofaneanesthesiausingasepticsurgicalprocedure.Aftersurgery,animalsarehousedindividually.Ondays3and4aftersurgery,OVX+Eanimalsareinjected(s.c.)with10μgof17β-estradiolbenzoatein100μLofsesameoilvehicle;OVX+Oanimalsreceiveoilvehicleateachinjectiontime.Forty-eighthoursafterthesecondestradiolorvehicleinjection,animalsarekilledbydecapitationandhippocampalslicesarepreparedfromtheirbrains.Gonadallyintactanimalsarekilledatrandomstagesoftheestrouscycle.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

• [1].WoolleyCS,etal.EstradiolincreasesthesensitivityofhippocampalCA1pyramidalcellstoNMDAreceptor-mediatedsynapticinput:correlationwithdendriticspinedensity.JNeurosci.1997Mar1;17(5):1848-59.

  [2].MermelsteinPG,etal.Estradiolreducescalciumcurrentsinratneostriatalneuronsviaamembranereceptor.JNeurosci.1996Jan15;16(2):595-604.

  [3].GirasoleG,etal.17beta-estradiolinhibitsinterleukin-6productionbybonemarrow-derivedstromalcellsandosteoblastsinvitro:apotentialmechanismfortheantiosteoporoticeffectofestrogens.JClinInvest.1992Mar;89(3):883-91.

  [4].WoolleyCS,etal.Estradiolmediatesfluctuationinhippocampalsynapsedensityduringtheestrouscycleintheadultrat.JNeurosci.1992Jul;12(7):2549-54.

  [5].WoolleyCS,etal.Rolesofestradiolandprogesteroneinregulationofhippocampaldendriticspinedensityduringtheestrouscycleintherat.JCompNeurol.1993Oct8;336(2):293-306.

272.38

C₁₈H₂₄O₂

50-28-2

RoomtemperatureincontinentalUS;mayvaryelsewhere

DMSO:≥150mg/mL

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

Purity:98.45%

SelectBatch:HY-B0141-14150HY-B0141-25250

DataSheet(122KB)SDS(389KB)

COA(94KB)HNMR(643KB)LCMS(139KB)

HandlingInstructions(1252KB)

• [1].WoolleyCS,etal.EstradiolincreasesthesensitivityofhippocampalCA1pyramidalcellstoNMDAreceptor-mediatedsynapticinput:correlationwithdendriticspinedensity.JNeurosci.1997Mar1;17(5):1848-59.

  [2].MermelsteinPG,etal.Estradiolreducescalciumcurrentsinratneostriatalneuronsviaamembranereceptor.JNeurosci.1996Jan15;16(2):595-604.

  [3].GirasoleG,etal.17beta-estradiolinhibitsinterleukin-6productionbybonemarrow-derivedstromalcellsandosteoblastsinvitro:apotentialmechanismfortheantiosteoporoticeffectofestrogens.JClinInvest.1992Mar;89(3):883-91.

  [4].WoolleyCS,etal.Estradiolmediatesfluctuationinhippocampalsynapsedensityduringtheestrouscycleintheadultrat.JNeurosci.1992Jul;12(7):2549-54.

  [5].WoolleyCS,etal.Rolesofestradiolandprogesteroneinregulationofhippocampaldendriticspinedensityduringtheestrouscycleintherat.JCompNeurol.1993Oct8;336(2):293-306.

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。

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