Description | Daidzeinisasoyisoflavone,whichactsasaPPARactivator. |
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IC50&Target | PPAR[1] |
InVitro | In3T3-L1ADIpocytes,Daidzeininversestheattenuationofadiponectingeneexpressionbyco-culture,andtheseeffectsareinhibitedbythePPAR-γspecificinhibitor.Daidzeinattenuatesthereductionofadiponectinexpressioninadipocytes,andaPPAR-γspecificinhibitorabrogatedthiseffect.DirectactivationofPPAR-αand-γbyDaidzeinisconfirmedbyaluciferasereporterassay.InHEK293Tcells,DaidzeinsignificantlyincreasesPPAR-αtranscriptionalactivityinaconcentration-dependentmanner.Althoughanobviousdose-dependencyisnotobservedinPPAR-γtranscriptionalactivity,DaidzeinalsosignificantlyincreasesPPAR-γtranscriptionalactivityoverasimilarrangeofconcentrationsatwhichDaidzeinenhancedPPAR-αtranscriptionalactivity,withamaximumincreaseat25μM[1].Daidzeinisasoyisoflavone,whichupregulatestheexpressionofAbcg1,anditpromotesaxonaloutgrowthinculturedhippocampalneuronsviaestrogenreceptorsignaling.Daidzeinisamajorcomponentofsoywithstructuralsimilaritytoestrogen.Itexertsananti-inflammatoryeffect,lowerslipidlevels,andincreasesmitochondrialbiogenesis.Asanactivatorofnuclearreceptorperoxisomeproliferator-activatedreceptors(PPARs),DaidzeinenhancestranscriptionofPPARs-dependentgenes,includingliverXreceptors(LXRs,Nr1hgenefamilyinmice).IncubationwithdifferentconcentrationsofDaidzein,from5to100μM,increasesAPOEtranscriptionalactivity[2]. |
InVivo | TreatingApoeKOmicewithDaidzeinincreasesLxrandAbca1geneexpressionat1monthafterstroke,showingthattheabsenceofApoEdoesnotinterferewithothercholesterolhomeostasisgeneticprograms.Therefore,thefindingssuggestthatDaidzein-inducedApoEupregulationisacriticalcomponentinfosteringfunctionalrecoveryinchronicstroke[2]. |
ClinicalTrial | ViewMoreCollapse |
References |
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PreparingStockSolutions |
Pleaserefertothesolubilityinformationtoselecttheappropriatesolvent. | ||||||||||||||||||||||||||
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CellAssay [1] | DaidzeinisdissolvedinDMSOandthendilutedwithappropriatemedia[1]. HEK293Tcellsareplatedon24-wellplatesatacelldensityofapproximately2.5×104cells/wellandaregrownto70-80%confluence.CellsarethentransientlytransfectedwithaPPAR-αorPPAR-γexpressionplasmid,andaplasmidcontainingtheluciferasegeneunderthecontrolofthreetandemPPARresponseelements(PPRE×3TK-luciferase)usinganX-tremeGENEHPDNATransfectionReagent.Renillaluciferasecontrolvectorsareco-transfectedtocontrolfortransfectionefficiency.Aftertransfection,cellsareculturedforanother24hinmediumcontainingDMSOorvariousconcentrations(6.25,12.5,25μM)ofDaidzein.Cellsarelysed,andluciferaseactivityismeasuredandexpressedasfoldinduction,thatisnormalizedtotheactivityoftherenillaluciferasecontrolplasmid[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly. | ||||||||||||||||||||||||||
AnimalAdmiNISTration [2] | Mice[2] References |
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