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.

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托烷司琼临床评价药物相关作用适应症托烷司琼CAS号:89565-68-4英文名称:Tropisetron英文同义词:icf205-930;TROPICACID;TROPISETRON;SS-TROPISETRON;BETA-TROPISETRON;Tropisetron(ICS205930);TROPISHTRONHYDROCHLORIDE;Indole-3-carbonylchloride;3-Tropanylindole-3-carboxylate;lαH，5Αh-Tropan-3α-ylindole-3-carboxylate中文名称:托烷司琼中文同义词:托普西隆;托普西龙;曲匹西龙;托烷司琼;Β-托烷司琼;CS-348;Β-内托烷司琼;吲哚-3-甲酰氯;Β-托烷司琼(光学异构体);Β-托烷司琼,托烷司琼异构体CBNumber:CB3236404分子式:C17H20N2O2分子量:284.35MOLFile:89565-68-4.mol化学性质安全信息用途供应商112化学性质安全信息用途供应商112托烷司琼化学性质熔点:201-202°C沸点:448.5±35.0°C(Predicted)密度:1.26储存条件:2-8°C溶解度:H2O:soluble形态:solid酸度系数(pKa):15.38±0.30(Predicted)颜色:whiteCAS数据库:Chemicalbook89565-68-4(CASDataBaseReference)安全信息WGKGermany:3托烷司琼化学药品说明书托烷司琼|药物应用信息托烷司琼性质、用途与生产工艺临床评价Sorbe等报道本品对含顺铂(剂量50～89mg/m2)化疗方案引起的急性呕吐完全控制率为63%。58例恶性肿瘤化疗所致恶心、呕吐者，应用托烷司琼或昂丹司琼8mg分别在同一病人前后2个化疗周期的第1d给药前30min静脉注射，并用地塞米松10mg静脉滴注。结果两药控制急性及迟发性恶心、呕吐的疗效基本相似，均可达81%～100%。本品对强致吐化疗药物顺铂的止吐疗效突出。药物相关作用饮食可略为延长本品的吸收。本品与利福平、苯巴比妥等肝酶诱导药同时使用，可加快代谢，故快代谢型者需增加剂量，慢者则不必。西咪替丁等肝酶抑制药对本品血药浓度无明显影响。适应症托烷司琼临床用于预防和治疗癌症化疗引起的恶心和呕吐。化学性质结晶，熔点201-202℃(二氯甲烷-乙酸乙酯)。单盐酸托烷司琼(TropisetronMonohydroehloride)：C17H20N2O2?HCI。[105826-92-4]。熔点283-285℃(分解)。用途有高效性和选择性的5-HT3受体拮抗剂。用于化疗所致的呕吐。用途为5-羟色胺拮抗药生产方法托品醇(I)和酰氯(Ⅱ)反应，可得托烷司琼。托烷司琼上下游产品信息上游原料托品醇下游产品

公司介绍

托烷司琼临床评价药物相关作用适应症托烷司琼CAS号:89565-68-4英文名称:Tropisetron英文同义词:icf205-930;TROPICACID;TROPISETRON;SS-TROPISETRON;BETA-TROPISETRON;Tropisetron(ICS205930);TROPISHTRONHYDROCHLORIDE;Indole-3-carbonylchloride;3-

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