MPTP-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEMPTPCat.No.:HY-W114750CASNo.:28289-54-5分⼦式:C₁₂H₁₅N分⼦量:173.25作⽤靶点:DopamineReceptor;Apoptosis作⽤通路:GPCR/GProtein;NeuronalSignaling;Apoptosis储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性MPTP(1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine)可透过⾎脑屏障的多巴胺(dopamine)神经毒素，MPTP可⽤于诱导帕⾦森综合症模型。MPTPMPP+的前体，可以诱导凋亡(apoptosis)。体外研究Pretreatmentwith50mM4-phenylpyridine,reducesIC50(concentrationfor50%inhibitionoftwitchamplitude)valuesofMPTPfrom53to18mMandd-tubocurarinefrom0.7to0.3mM,respectively,inmousephrenicnerve-diaphragm[2].体内研究MPTPcanbeusedinanimalmodelingtocreateParkinson'sdiseasemodels.MPTPreplicatesnaturallyoccurringneurodegenerationandisusefulforstudyingdopaminergicneuronaldegeneration,mitochondrialdysfunction,andneuroinflammation.Afterinjection,MPTPisrapidlymetabolizedtoMPP+,whichhasaserumhalf-lifeofapproximately6daysinsheep.InductionofParkinsonismmodel[4][5][6][7]BackgroundMPTPisfreetocrosstheblood-brainbarrierandenterthebrain,whereitismetabolizedbymonoamineoxidaseB(MAO-B)inastrocytesintoMPP+,itsactive&toxicform.MPP+istakenupbydopamineneuronsviaadopaminetransporter(DAT),blockingComplexIintheelectrontransportchainofmitochondria,triggeringoxidativestressandmitochondrialbreakdown,andfinallyleadingtoneuronapoptosis.InParkinson'sdisease,itisthelossofneuronsinthesubstantianigra,thedopamine-producingpartofthesubstantianigrostriatumsystem,thatcausesthedisease.DuetothetoxiceffectsofMPTP,itwillcausethedeathofdopamineneuronsinthesubstantianigra,causingsymptomssimilartoParkinson'sdisease.SpecificModelingMethodsMice:C57BL/6•male•8-12week-old(period:2weeks),oldermicemaybemoresensitiveAdministration:Acutemodel:14-20mg/kg•ip•4timesaday,twohoursapartSub-acutemodel:20-30mg/kg•ip•oncedailyfor5daysNote1.Afteradministration,wecanobserve1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEwhetherthemicehavesymptomssuchasreducedactivity,staggeringwalking,twitching,friedhair,increasedurination,etc.Thisbehaviormaylastfor24-48hours,afterwhichthemicebehavebasicallynormally.2.MPTPisusuallysoldasMPTPhydrochloride.ThemolecularweightofMPTPhydrochlorideis209.7.Therefore,itisrecommendedtotakeintoaccountthepresenceofhydrochloride(HCl)whenpreparinginjectablesolutions.HClhasamolecularweightof35.4andaccountsfor17%ofMPTP.Thus,ifa20mg/kgdoseofMPTPistobeprepared,theMPTPhydrochloridedoseadministeredis20mgkg*1.17%=23.4mg/kg.3.Ifmultipleinjectionsaregivenwithin1day,itisbesttoalternatetheinjectionsonbothsides.Ifinjectedeveryday,itshouldbedoneatthesametime.Beforeeachinjection,themiceneedtobeweighedandthedosagevolumeshouldbeadjusted.4.ModelingmicemaynotshowbehavioraldefectsofParkinson'sdisease.Micemayshowindividualdifferences,andthesuccessrateofmodelingisgenerallydifficulttoreach100%.ThereforenigrostriataldamageassociatedwithgliosisshouldbemainlymonitoredinMPTPmousestudies.5.Highdrugdosage/miceweighinglessthan22g/mixingofdrugsfromdifferentbatches/micenotadaptinginadvance/animalroombeingtoocoldmayresultinanumberofdeaths.Itisrecommendedthatthenumberofanimalsineachgroupbeincreased,andadjusttotheoptimaldoseaccordingtoexperimentalconditions.ModelingIndicatorsNigrostriatalinjury:Tyrosinehydroxylaseinthesubstantianigraandstriatumisreducedaftersuccessfulmodeling(IHC,IF,WB,etc.);Othermarkers:reductionofbrainneurotransmitters(DA,DOPAC,5-HT,HVA,etc.)(detectedbyHPLC);Nigrostriatalmicroglia(IBA1+cells)andastrocytes(GFAP+cells)areactivated,andthenumberofα-synaggregatesinthesubstantianigra.CorrelatedProduct(s):/OppositeProduct(s):HY-W013494PROTOCOLAnimalForthepreparationoftheLPSratmodelandtheMPTPmousemodel,thetreatmentsoftheanimalsareAdministration[3]performed.Briefly,adultratsreceiveunilateralinjectionsofLPS(0.5μLof10μg/μLdilutedin0.9%saline)intothemedialforebrainbundle(MFB)atthefollowingcoordinates,AP-4.2mm,L1.5mm,andV7.8mm,andintothecontralateralsidewiththesamevolumeof0.9%saline.AdultmiceareadministeredintraperitonealinjectionsofMPTPof25mg/kgperdayforfivecontinuousdays,andthesamevolumeofsalineisinjectedasacontrol.Alltheanimalsaresacrificedatweek1,2,3,or4aftertheLPSorMPTPinjections.Thebrainsamplesarecollectedforthesubsequentimmunohistochemistryandwesternblotexperiments.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献•SignalTransductTargetTher.2021Feb24;6(1):77.•ChemEngJ.2024Sep20.•JNanobiotechnology.2024Sep14;22(1):567.•JNeuroinflammation.2024Apr12;21(1):92.•FoodResInt.2025Feb:201:115590.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemESeemorecustomervalidationsonwww.MedChemEREFERENCES[1].LangstonJW,IrwinI.MPTPNeurotoxicity:AnOverviewandCharacterizationofPhasesofToxicity.II.SelectiveAccumulationofMPPintheSubstantiaNigra:AKeytoNeurotoxicity(Question).LifeSci.,1985,36,No.3,201-12.[2].HsuKS,etal.PotentiationofMPTPby4-PhenylpyridineontheNeuromuscularBlockadeinMousePhrenicNerve-Diaphragm.Neuropharmacology,1993,32,No.9,877-83.[3].SunXL,etal.Gas1up-regulationisinducibleandcontributestocellapoptosisinreactiveastrocytesinthesubstantianigraofLPSandMPTPmodels.JNeuroinflammation.2016Jul8;13(1):180.[4].Jackson-LewisV,PrzedborskiS.ProtocolfortheMPTPmousemodelofParkinson'sdisease.NatProtoc.2007;2(1):141-51.[5].Rabaneda-LombarteN,etal.TheCD200R1microglialinhibitoryreceptorasatherapeutictargetintheMPTPmodelofParkinson'sdisease.JNe