Urolithin-A-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEUrolithinACat.No.:HY-100599CASNo.:1143-70-0分?式:C??H?O?分?量:228.2作?靶點(diǎn):DrugMetabolite;ReactiveOxygenSpecies;DNA/RNASynthesis;Autophagy;Apoptosis;EndogenousMetabolite作?通路:MetabolicEnzyme/Protease;Immunology/Inflammation;NF-κB;CellCycle/DNADamage;Autophagy;Apoptosis儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實(shí)驗(yàn)DMSO:30mg/mL(131.46mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM4.3821mL21.9106mL43.8212mL5mM0.8764mL4.3821mL8.7642mL10mM0.4382mL2.1911mL4.3821mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲備液；?旦配成溶液，請分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲存時(shí)，請?jiān)?個(gè)?內(nèi)使?，-20°C儲存時(shí)，請?jiān)?個(gè)?內(nèi)使?。體內(nèi)實(shí)驗(yàn)請根據(jù)您的實(shí)驗(yàn)動物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請先按照InVitro?式配制澄的儲備液，再依次添加助溶劑：(為保證實(shí)驗(yàn)結(jié)果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)天使?；以下溶劑前顯?的百分?指該溶劑在您配制終溶液中的體積占?；如在配制過程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1.請依序添加每種溶劑：0.5%CMC/salinewater1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESolubility:5mg/mL(21.91mM);Suspendedsolution;Needultrasonic2.請依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.5mg/mL(10.96mM);Clearsolution3.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:2.5mg/mL(10.96mM);Suspendedsolution;Needultrasonic4.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(10.96mM);ClearsolutionBIOLOGICALACTIVITY?物活性UrolithinA，鞣花酸的腸道微?物代謝產(chǎn)物，具有抗炎、抗增殖和抗氧化的特性。UrolithinA誘導(dǎo)?噬和凋亡，抑制細(xì)胞周期進(jìn)程，抑制DNA合成。IC50&TargetHumanEndogenousMetabolite體外研究MicromolarurolithinAconcentrationsinducesbothautophagyandapoptosis.UrolithinAsuppressescellcycleprogressionandinhibitedDNAsynthesisinhumansw620colorectalcancercells[2].UrolithinAshowsantiproliferativeeffectsandinhibitsT24andCaco-2cellgrowthwithIC50sof43.9and49μM,respectively[3].UrolithinAexertsadose-andtime-dependentsignificantarrestatG2/MandSphasesaftertreatmentswith50and100μMat24and48hcomparedtocontrolcells.Itinducescellapoptosiswith50and100μM[4].UrolithinAshowspotentantiproliferativeactivityonHepG2cells.WhencelldeathisinducedbyUrolithinA,theexpressionofβ-catenin,c-MycandCyclinD1aredecreasedandTCF/LEFtranscriptionalactivationisnotablydown-regulated.UrolithinAalsoincreasesproteinexpressionofp53,p38-MAPKandcaspase-3,butsuppressesexpressionofNF-κBp65andotherinflammatorymediators[5].體內(nèi)研究Thevolumeofpawedemaisreducedat1hafteroraladministrationofurolithinA.Inaddition,plasmaintreatedmiceexhibitedsignificantoxygenradicalantioxidantcapacity(ORAC)scoreswithhighplasmalevelsoftheunconjugatedformat1hafteroraladministrationofurolithinA[6].PROTOCOLCellAssay[2]HumancoloncancercellsHT-29aretreatedfor24and48hat100and50μMofUrolithinAandIsoUrolithinAaglyconesandtheirglucuronideconjugates.CellviabilityandproliferationaremeasuredusingaTC10automatedcellcounterwiththeadditionofTrypanblueforviabilitydetermination.IC50valuesaredeterminedbyMTTassay[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice:PawedemaisinducedintherighthindpawofICRmicebythesubcutaneousinjectionof1%λ-Administration[4]carrageenaninpysiologicalsaline(50μL).Theinflammationlevelisquantifiedbythevolumeofpawedema.UrolithinAdissolvedin0.5%carboxymethylcellulosesuspensionisorallyadministeredtothemiceat1or6hbeforecarrageenaninjection.Theanti-inflammatoryeffectsofurolithinAoncarrageenan-inducededemain2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEmiceareanalyzed[4].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?JNanobiotechnology.2022Mar19;20(1):149.?CommunBiol.2022Jun22;5(1):616.?WorldJStemCells.2021Dec26;13(12):1928-1946.?CellStressChaperones.2021Mar5.?ResearchSquarePreprint.2021Oct.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].GongZ,etal.UrolithinAattenuatesmemoryimpairmentandneuroinflammationinAPP/PS1mice.[2].ZhaoW,etal.Metaboliteofellagitannins,urolithinAinducesautophagyandinhibitsmetastasisinhumansw620colorectalcancercells.MolCarcinog.2018Feb;57(2):193-200.[3].QiuZ,etal.Invitroantioxidantandantiproliferativeeffectsofellagicacidanditscolonicmetabolite,urolithins,onhumanbladdercancerT24cells.FoodChemToxicol.2013Sep;59:428-37.[4].González-SarríasA,etal.Antiproliferativeactivityoftheellagicacid-derivedgutmicrobiotaisourolithinAandcomparisonwithitsurolithinAisomer:theroleofcellmetabolism.EurJNutr.2017Mar;56(2):831-841.[5].WangY,etal.InvitroantiproliferativeandantioxidanteffectsofurolithinA,thecolonicmetaboliteofellagicacid,onhepatocellularcarcinomasHepG2cells.ToxicolInVitro.2015Aug;29(5):1107-15.[6].IshimotoH,etal.Invivoanti-inflammatoryandantioxidantpropertiesofellagitanninmetaboliteurolit