Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemENaringinDihydrochalconeCat.No.:HY-N0119CASNo.:18916-17-1Synonyms:NaringinDC分?式:C??H??O??分?量:582.55作?靶點:NF-κB作?通路:NF-κB儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實驗DMSO:≥100mg/mL(171.66mM)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制備儲備液1mM1.7166mL8.5830mL17.1659mL5mM0.3433mL1.7166mL3.4332mL10mM0.1717mL0.8583mL1.7166mL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，請在6個?內(nèi)使?，-20°C儲存時，請在1個?內(nèi)使?。體內(nèi)實驗請根據(jù)您的實驗動物和給藥?式選擇適當?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：(為保證實驗結(jié)果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當保存；體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)配，當天使?；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)1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE1.請依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥10mg/mL(17.17mM);Clearsolution2.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(4.29mM);Clearsolution3.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥10mg/mL(17.17mM);ClearsolutionBIOLOGICALACTIVITY?物活性NaringinDihydrochalcone由柚?苷衍?的?造甜味劑。柚?苷從番茄，葡萄柚和許多其他柑橘類?果中獲得的主烷酮糖苷。柚?素表現(xiàn)出抗氧化，抗炎和抗細胞凋亡等?物活性。Naringin可抑制NF-κB信號通路。IC50&TargetNF-κB體外研究NaringinsuppressesNF-κBsignalingpathwayactivation.Naringenininhibitshighglucose-inducedproliferation,inflammatoryreactionandoxidativestressinjuryinHBZY-1cells[1].NaringininhibitsAGScancercellproliferationinadose-andtime-dependentmanner.PhosphorylationofPI3Kanditsactivateddownstreamtargetsp-Aktandp-mTORaresignificantlydecreasedat2mMinNaringin-treatedAGScells.NaringininducesautophagiccelldeathinAGScells.NaringinactivatedtheautophagyrelatedproteininAGScells[2].NaringinprotectsPC12cellsfrom3-NPneurotoxicity.Thelactatedehydrogenasereleaseisdecreaseduponnaringintreatmentin3-NP-inducedPC12cells.Naringintreatmentenhancestheantioxidantdefensebyincreasingtheactivitiesofenzymaticantioxidantsandthelevelofreducedglutathione[3].體內(nèi)研究Treatmentwithnaringinsignificantlyalleviatesrenalinjuryindiabeticratsandincreasesdiabeticratsbodyweightsignificantly.Administrationofnaringineffectivelyalleviatesthecollagendepositionandrenalinterstitialfibrosisindiabeticrats.TreatmentwithnaringincouldresultindecreasedlevelsofROSandMDAandincreasedactivitiesofSODandGSH-Px[1].Oraladministrationofnaringinsignificantlyimprovesthelearningandmemoryabilities.Naringinsignificantlyenhancesinsulinsignalingpathway[3].PROTOCOLCellAssay[1]HBZY-1cellsareplatedinto96-wellplatesandpretreatedwithvariousconcentrations(1,5,10,25,50,100μM)ofnaringinfor2h.Thencellsaretreatedwith30mMglucosefor24h.Thecontrolgroupisaddedsterilenormalsalineinthesamevolume.Aftertreatment,allthewellsareincubatedwith20μlof5mg/mlMTTfor4hat37°C.Subsequently,100μlofDMSOareusedtodissolvetheformedformazancrystalsafterremovalofthesupernatant.Theresultisrecordedat490nmonamicroplatereader[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalRats:Theratsarerandomlydividedintosixgroups:control,naringin(80mg/kg),STZ,STZ+naringin(20Administration[1][4]mg/kg),STZ+naringin(40mg/kg),STZ+naringin(80mg/kg).TheratsintheSTZandSTZ+naringingroupsareintraperitoneallyinjectedwithSTZ(65mg/kg).Thecontrolandnaringingroupsareintraperitoneally2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEinjectedwith0.1Mcitratebufferofsamevolume.AfterinjectionofSTZfor3and5days,bloodglucoselevelsaremeasuredbytailveinpuncturebloodsampling[1].Mice:Sixty4-week-oldmalemicearerandomizedintofourgroupsandfedfor20weekswitheithercontroldietorhigh-fatdietchow.Micearedosedwith100mg/kgofnaringindaily.Micebodyweightandfoodintakeareweeklymeasured.Followingbehavioralassessment,animalsaredeeplyanesthetizedwithisofluraneandsacrificedbydecapitationafterfastingforatleast5h.Theirplasmaiscollectedforfurtheranalysis[4].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻?ActaPharmSinB.2021Jan;11(1):143-155.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].ChenF,etal.NaringinAlleviatesDiabeticKidneyDiseasethroughInhibitingOxidativeStressandInflammatoryReaction.PLoSOne.2015Nov30;10(11):e0143868.[2].RahaS,etal.Naringininducesautophagy-mediatedgrowthinhibitionbydownregulatingthePI3K/Akt/mTORcascadeviaactivationofMAPKpathwaysinAGScancercells.IntJOncol.2015Sep;47(3):1061-9.[3].KulasekaranG,etal.Neuroprotectiveefficacyofnaringinon3-nitropropionicacid-inducedmitochondrialdysfunctionthroughthemodulationofNrf2signalingpathwayinPC12cells.MolCellBiochem.2015Nov;409(1-2):199-211.[4].WangD,etal.NaringinImprovesNeuronalInsulinSignaling,BrainMitochondrialFunction,andCognitiveFunctioninHigh-FatDiet-Induc