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Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemETempolCat.No.:HY-100561CASNo.:2226-96-2Synonyms:4-Hydroxy-TEMPO分?式:C?H??NO?*分?量:172.24作?靶點(diǎn):ReactiveOxygenSpecies;Autophagy作?通路:Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB;Autophagy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)H2O:5.56mg/mL(32.28mM;ultrasonicandwarmingandheatto60°C)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM5.8059mL29.0293mL58.0585mL5mM1.1612mL5.8059mL11.6117mL10mM0.5806mL2.9029mL5.8059mL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(guò)程中出現(xiàn)沉淀、析出現(xiàn)象,可以通過(guò)加熱和/或超聲的?式助溶)1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE1.請(qǐng)依序添加每種溶劑:PBSSolubility:25mg/mL(145.15mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY?物活性Tempol?種超氧化物歧化酶(SOD)類似物,可有效中和活性氧(ROS)。IC50&TargetROS[1]體外研究TempolsignificantlyattenuatesH2O2-mediateddecreaseinmitochondrialrespirationandincreaseinLDHreleasefromratPTcells,indicatingareductionincellinjuryanddeath.ThebeneficialactionsofTempolaresimilartothoseobtainedusingtheFe2+chelatorDEF.However,coadministrationofDEFandTempoldoesnotproduceanyadditionalbeneficialactionsagainstrenalischemia/reperfusioninjuryoragainstoxidativestress-mediatedPTcellinjury/death[2].體內(nèi)研究SOD-mimeticTempolisabletomimicresveratrol’seffectsonheartfunction.Tempolisadministereddailybygavage.MicetreatedwithMetorTmphaddecreasedPRandQTcintervalsandincreasedheartratescomparedtoperoralvehicle(VEH).TheseresultsaresimilartothatobtainedbytreatmentwithRSV.Pre-andpost-treatmentprofilesofindividualmiceareillustrated[1].Tempol,amembrane-permeableradicalscavenger,reducesoxidantstress-mediatedrenaldysfunctionandinjuryintherat.Tempolsignificantlyreducestheincreaseinurea,creatinine,γGT,AST,NAG,andFENaproducedbyrenalischemia/reperfusion,suggestinganimprovementinbothrenalfunctionandinjury.TempolalsosignificantlyreduceskidneyMPOactivityandMDAlevels,indicatingareductioninPMNinfiltrationandlipidperoxidation,respectively.Tempolreducesthehistologicevidenceofrenaldamageassociatedwithischemia/reperfusionandcausedasubstantialreductioninthestainingfornitrotyrosineandPARS,suggestingreducednitrosativeandoxidativestress[2].PROTOCOLCellAssay[2]ToinvestigatetheeffectofTempol,DEF,andDEFcoadministeredwithTempolonH2O2-mediatedcellinjuryanddeath,confluentculturesofPTcellsarepreincubated(10minat37°C)withTempol(0.03to10mM),DEF(0.03to10mM),orDEF(3mM)incombinationwithTempol(3mM).TherangesofconcentrationsofTempolandDEFarebasedonthosepreviouslyshowninthislaboratorytoreduceonH2O2-mediatedcellinjuryanddeathin(1)culturedratcardiacmyoblasts(Tempol)and(2)primaryculturesofratPTcells(DEF).PTcellculturesarethenincubatedwithH2O2(1mM)forfourhours,afterwhichcellularinjuryanddeathareassessed.Uponcompletionofincubations,cellularinjuryanddeathareassessedusingthespectrophotometricassaysdescribedlaterinthisarticle[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice[1]Administration[1][2]FemaleormaleBALB/cmice(5-7weeksofage)areused.Miceareinfectedintraperitoneally(i.p.)with102bloodtrypomastigoteformsofthetypeIColombianstrainofT.cruzi.Treatmentsareperformeddailyfor302/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEdaysfromtheestablishmentofCCC(60dpi)byi.p.injectionof15mg/kgtrans-resveratrol(10%ethanol/PBS),vehicle(10%ethanol/PBS),5mg/KgEX527(0.1%DMSO),orperoraladministrationof40mg/KgResveratrol(10%ethanol-PBS),500mg/kgMetformin(dissolvedinwater),100mg/kgTempol(dissolvedinwater),Benznidazole(25mg/Kg,dissolvedinwater)andvehicle(wateror10%ethanol-PBS).Rats[2]83maleWistarratsweighing230to320gareused.Uponcompletionofsurgicalprocedures,theanimalsarerandomlyallocatedtotheeightgroups.Atoneminutebeforecommencementofreperfusion,animalsreceivedabolusinjectionofeithervehicle(saline,4mL/kg,IV),Tempol(30mg/kginsaline,IV),DEF(40mg/kginsaline,IV),orDEF(40mg/kginsaline,IV)incombinationwithTempol(30mg/kginsaline,IV).Thecorrespondinggroupsthenreceivedacontinuousinfusionofoneofthefollowingthroughoutthereperfusionperiod:vehicle(saline,4mL/kg/h,IV),Tempol(30mg/kg/hinsaline,IV),DEF(40mg/kg/hinsaline,IV),orTempolandDEFincombination(30and40mg/kg/h,respectively,insaline,IV).ToelucidatetheeffectsofTempolorDEFoncardiovascularhemodynamicsandorganfunctioninsham-operatedrats,respectivegroupsofanimalsreceivedthetreatmentsdescribedpreviouslyinthisarticleandasoutlined.TheconcentrationofTempoladministeredinvivoisbasedonthosepreviouslydemonstratedbyustoprovidesignificantprotectionagainstmyocardialischemia/reperfusioninjuryinaninvivoratmodel.Similarly,theconcentrationofDEFusedisidenticaltothatwhichwehavepreviouslyusedtoprovidesignificantprotectionagainsthepaticischemia/reperfusioninjuryininvivoratandrabbitmodels.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?RedoxBiol.October2021,102115.?Cells.2022Apr2;11(7):1196.?OxidMedCellLongev.05Oct2021.?JNutrBiochem.2021Oct1

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