Naringin-Dihydrochalcone-Naringin-DC-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemENaringinDihydrochalconeCat.No.:HY-N0119CASNo.:18916-17-1Synonyms:NaringinDC分⼦式:C₂₇H₃₄O₁₄分⼦量:582.55作⽤靶点:NF-κB作⽤通路:NF-κB储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验DMSO:≥100mg/mL(171.66mM)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制备储备液1mM1.7166mL8.5830mL17.1659mL5mM0.3433mL1.7166mL3.4332mL10mM0.1717mL0.8583mL1.7166mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；⼀旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存⽅式和期限：-80°C,6months;-20°C,1month。-80°C储存时，请在6个⽉内使⽤，-20°C储存时，请在1个⽉内使⽤。体内实验请根据您的实验动物和给药⽅式选择适当的溶解⽅案。以下溶解⽅案都请先按照InVitro⽅式配制澄的储备液，再依次添加助溶剂：(为保证实验结果的可靠性，澄的储备液可以根据储存条件，适当保存；体内实验的⼯作液，建议您现⽤现配，当天使⽤；以下溶剂前显⽰的百分⽐指该溶剂在您配制终溶液中的体积占⽐；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的⽅式助溶)1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE1.请依序添加每种溶剂：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥10mg/mL(17.17mM);Clearsolution2.请依序添加每种溶剂：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(4.29mM);Clearsolution3.请依序添加每种溶剂：10%DMSO>>90%cornoilSolubility:≥10mg/mL(17.17mM);ClearsolutionBIOLOGICALACTIVITY⽣物活性NaringinDihydrochalcone由柚⽪苷衍⽣的⼈造甜味剂。柚⽪苷从番茄，葡萄柚和许多其他柑橘类⽔果中获得的主烷酮糖苷。柚⽪素表现出抗氧化，抗炎和抗细胞凋亡等⽣物活性。Naringin可抑制NF-κB信号通路。IC50&TargetNF-κB体外研究NaringinsuppressesNF-κBsignalingpathwayactivation.Naringenininhibitshighglucose-inducedproliferation,inflammatoryreactionandoxidativestressinjuryinHBZY-1cells[1].NaringininhibitsAGScancercellproliferationinadose-andtime-dependentmanner.PhosphorylationofPI3Kanditsactivateddownstreamtargetsp-Aktandp-mTORaresignificantlydecreasedat2mMinNaringin-treatedAGScells.NaringininducesautophagiccelldeathinAGScells.NaringinactivatedtheautophagyrelatedproteininAGScells[2].NaringinprotectsPC12cellsfrom3-NPneurotoxicity.Thelactatedehydrogenasereleaseisdecreaseduponnaringintreatmentin3-NP-inducedPC12cells.Naringintreatmentenhancestheantioxidantdefensebyincreasingtheactivitiesofenzymaticantioxidantsandthelevelofreducedglutathione[3].体内研究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—您⾝边的抑制剂⼤师www.MedChemEinjectedwith0.1Mcitratebufferofsamevolume.AfterinjectionofSTZfor3and5days,bloodglucoselevelsaremeasuredbytailveinpuncturebloodsampling[1].Mice:Sixty4-week-oldmalemicearerandomizedintofourgroupsandfedfor20weekswitheithercontroldietorhigh-fatdietchow.Micearedosedwith100mg/kgofnaringindaily.Micebodyweightandfoodintakeareweeklymeasured.Followingbehavioralassessment,animalsaredeeplyanesthetizedwithisofluraneandsacrificedbydecapitationafterfastingforatleast5h.Theirplasmaiscollectedforfurtheranalysis[4].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献•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