Bradykinin-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEBradykininCat.No.:HY-P0206CASNo.:58-82-2分?式:C??H??N??O??分?量:1060.21Sequence:Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-ArgSequenceShortening:RPPGFSPFR作?靶點(diǎn):BradykininReceptor;EndogenousMetabolite;Ser/ThrProtease作?通路:GPCR/GProtein;MetabolicEnzyme/Protease儲(chǔ)存?式:Powder-80°C2years-20°C1yearInsolvent-80°C6months-20°C1monthBIOLOGICALACTIVITY?物活性Bradykinin由激肽釋放酶-激肽系統(tǒng)產(chǎn)?的活性肽。它炎癥調(diào)節(jié)因?，也被認(rèn)為?種?管和腎功能以及神經(jīng)調(diào)節(jié)因?。IC50&TargetBradykininB2Receptor(B2R)HumanEndogenousMetabolite體外研究BradykininisapotentvasodilatorpeptidethatexertsitsvasodilatoryactionthroughstimulationofspecificendothelialB2receptors,therebycausingthereleaseofprostacyclin,NO,andEDHF[1].Bradykininhasbeenreportedtobeinvolvedintheprogressionofmanytypesofcancer.Bradykinintreatmentpromotestheinvasionandmigrationofcolorectalcancercells.BradykinintreatmentstimulatesERK1/2activationandIL-6production[2].ExogenousbradykininmarkedlyinhibitsTFexpressioninmRNAandproteinlevelinducedbyLPSinadose-dependentmanner.TheNOsynthaseantagonistL-NAMEandPI3KinhibitorLY294002dramaticallyabolishtheinhibitoryeffectsofbradykininontissuefactorexpression[3].體內(nèi)研究Applicationof1μMbradykinintotheovaryproducessignificantdecreasesinheartrateandmeanarterialpressure.Invagotomizedanimals,applicationof1μMbradykinintotheovaryproducesbradycardiaandhypotensionsimilartotheresponsesevokedwhenvagalinnervationisintact[4].Vascularbradykinincanimprovepancreaticmicrocirculationandhemorheologyinratswithsevereacutepancreatitis.Thepancreatic1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEmicrocirculatorybloodflowvolumeandvelocityinthevascularbradykinintreatmentgroupincreasesgraduallyafter48h[5].PI3K/AktsignalingpathwayactivationinducedbybradykininadministrationreducestheactivityofGSK-3βandMAPK,andreducesNF-x03BA;Blevelinthenucleus,therebyinhibitingTFexpression.Consistentwiththis,intraperitonealinjectionofC57/BL6micewithbradykininalsoinhibitsthethrombusformationinducedbyligationofinferiorvenacava[3].PROTOCOLCellAssay[2]SW480cellsarepretreatedwithdifferentconcentrationsofbradykinin(0,0.1,0.5,1μM),andthensubjectedtoinvasionandmigrationassays[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalRats:Bradykininacetateisappliedtopicallytothesurfaceoftheovarywithathinpieceofcotton(7×7mmAdministration[3][4]square)soakedwiththesolution.Afterapplicationfor30s,thecottonisremoved.Eachofthestimuliisdeliveredtotheanimalafterobservingstabilizationofheartrateandmeanarterialpressure[4].Mouse:Micearerandomlydividedinto3groups:Sham,ModelandBradykinin.Beforesurgicalprocedure,themiceofbradykiningroupareintraperitoneallyinjectedwithbradykinin(10mg/kg/d)onceadayforthreedays.Afterligation,themicereceivebradykinininjectionforanothertwodaysandanalgesictherapyisperformedusingbuprenorphineat0.1mg/kgbodyweightfor3days.Themiceinothergroupsreceiveequalsalineascontrol[3].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?AnalChem.2022Apr26;94(16):6363-6370.?iScience.21October2022.?ACSChemNeurosci.2021Jun29.?SLASDiscov.2018Nov1:2472555218810323.?JAmSocMassSpectrom.2020Jul5.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].HornigB,etal.Roleofbradykinininmediatingvasculareffectsofangiotensin-convertingenzymeinhibitorsinhumans.Circulation.1997Mar4;95(5):1115-8.[2].WangG,etal.BradykininstimulatesIL-6productionandcellinvasionincolorectalcancercells.OncolRep.2014Oct;32(4):1709-14.[3].DongR,etal.ExogenousBradykininInhibitsTissueFactorInductionandDeepVeinThrombosisviaActivatingtheeNOS/Phosphoinositide3-Kinase/AktSignalingPathway.CellPhysiolBiochem.2015;37(4):1592-606.[4].UchidaS,etal.Afferentfibersinvolvedinthebradykinin-inducedcardiovascularreflexesfromtheovaryinrats.AutonNeurosci.2015Dec;193:57-62.[5].LiuLT,etal.Effectofvascularbradykininonpancreaticmicrocirculationandhemorheologyinratswithsevereacutepancreatitis.EurRevMedPharmacolSci.2015;19(14):2646-50.2/3MasterofBioactiveMolecules—您?邊