Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemETroxerutinCat.No.:HY-N0139CASNo.:7085-55-4Synonyms:Trihydroxyethylrutin分?式:C??H??O??分?量:742.68作?靶點(diǎn):NOD-likeReceptor(NLR)作?通路:Immunology/Inflammation儲(chǔ)存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實(shí)驗(yàn)DMSO:100mg/mL(134.65mM;Needultrasonicandwarming)H2O:≥50mg/mL(67.32mM)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM1.3465mL6.7324mL13.4647mL5mM0.2693mL1.3465mL2.6930mL10mM0.1346mL0.6732mL1.3465mL請(qǐng)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(chǔ)備液；?旦配成溶液，請(qǐng)分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?，-20°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請(qǐng)先按照InVitro?式配制澄的儲(chǔ)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(chǔ)備液可以根據(jù)儲(chǔ)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1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1.請(qǐng)依序添加每種溶劑：0.5%CMC-Na/salinewaterSolubility:24mg/mL(32.32mM);Clearsolution;Needultrasonic2.請(qǐng)依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.5mg/mL(3.37mM);Clearsolution3.請(qǐng)依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(3.37mM);Clearsolution4.請(qǐng)依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(3.37mM);ClearsolutionBIOLOGICALACTIVITY?物活性Troxerutin也被稱為維?素P4，天然?物類酮蘆丁的三羥?化衍?物，其可抑制活性氧(ROS)的產(chǎn)?并抑制ER應(yīng)激介導(dǎo)的NOD活化。IC50&TargetROS[1],NOD[2]體外研究TheresultsrevealthatthemaximumprotectiveeffectagainstROSinducedcelldamageintheHDPcellsoccursfollowingpretreatmentwith10μMTroxerutin.TreatmentwithH2O2alonedecreasescellviabilityto77.33±2.44%;however,pretreatmentwith10μMTroxerutinmaintainscellviabilityat90.88±2.24%followingH2O2exposure(P2O2aloneincreasesthelevelofROSto46.36±2.33%.ThecellspretreatedwithTroxerutinare19.92±1.95%DCF-positivefollowingH2O2treatment,indicatingthatTroxerutinreducestheH2O2-inducedproductionofROSintheHDPcells[1].體內(nèi)研究Troxerutineffectivelylowersbodyweightandobesity-relatedmetabolicparametersinhigh-fatdiet(HFD)-treatedmice.OraladministrationofTroxerutinnotablyinhibitsthoseliverinjuriesinHFD-treatedmice,restoresglucoseintoleranceandinsulinsignaling,anddiminisheshepaticgluconeogenesisinHFD-treatedmice.TroxerutinremarkablyinhibitsthenucleartranslocationofNF-κBp65,aswellastheexpressionsofitstargetgenes,intheliversofHFD-treatedmice.Troxerutinalsodepressesendoplasmicreticulum(ER)stress-mediatedNucleotideoligomerizationdomain(NOD)activationinHFD-treatedmouselivers[2].LipiddepositionsintunicaintimaeandtunicamediaareattenuatedinTroxerutin-treateddiabeticratscomparewithuntreateddiabeticrats.StructuraldisarrangementanddeformityofsmoothmusclecellsinaortictissueofTroxerutin-treateddiabeticratsareconsiderablylowerthanhistologyofuntreateddiabeticaorta.AdministrationofTroxerutinforfourweekstodiabeticratssignificantlyreducesthelevelofmalondialdehyde(MDA)comparetothatofuntreateddiabeticrats(P[3].PROTOCOLCellAssay[1]Thecellsareplatedatadensityof4×103/wellina96-wellplate.At70to80%confluence,thecellsaretreatedwithTroxerutinatconcentrationsrangingbetween0and60μMfor24hat37°C.Subsequently,10μLwatersolubletetrazoliumsaltassaysolutionisaddedtoeachwelland,followingincubationfor30minat37°C,theopticaldensityismeasuredat490nmusingareader.ToexamineTroxerutinmediatedROS2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEprotection,thecellsarepretreatedwithTroxerutinatthefollowingconcentrations:0,5,10and15μMfor8h.Subsequently,750μMH2O2isaddedtoeachwell.Followingincubationfor24hat37°C,cellviabilityisevaluatedusinganCellViabilityAssaykit.Thelevelofcellviability(%)isnormalizedtothatof0.1%dimethyl-sulfoxide(DMSO)-treatedcells.Eachexperimentisrepeatedatleastthreetimes[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalThirtytwoadultmaleWistarratsweighing250to300gramsareusedinthisstudy.TheanimalsareAdministration[3]randomlydividedintofourgroups(n=8/each)as:groupI:control(C),groupII:controlwithTroxerutin(C+TXR),groupIII:diabetic(D),andgroupIV:diabeticwithTroxerutin(D+TXR).Thecontrolratsarereceivedthesameamountofcitratebufferalone.Developmentofdiabetesisconfirmedbymeasuringbloodglucoselevels,72hourslater.Animalswithbloodglucoselevelshigherthan16.65mM(300mg/dL)areconsidereddiabeticandthosewithbloodglucoselevelslowerthanthisvalueareexcludedfromtheexperiment.Troxerutin(150mg/kg/day)isadministeredorally,oncedailyforfourweeks.After10weeksofinductionofdiabetes,diabeticanimalsaswellasthetime-matchedcontrolsarekilledandaorticsamplesarecollected[3].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.REFERENCES[1].LimKM,etal.AnalysisofchangesinmicroRNAexpressionprofilesinresponsetothetroxerutin-mediatedantioxidanteffectinhumandermalpapillacells.MolMedRep.2015Aug;12(2):2650-60.[2].ZhangZ,etal.TroxerutinAttenuat