Notch通路对高糖诱导人晶状体上皮细胞凋亡中P53、BAX作用的研究-豆柴文库

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Notch通路对高糖诱导人晶状体上皮细胞凋亡中P53、BAX作用的研究
Title:RoleofNotchSignalingPathwayinHighGlucoseInducedApoptosisofHumanLensEpithelialCells:FocusonP53andBAX
Abstract:
Diabeticcataractisacommoncomplicationofdiabetesmellitus,characterizedbyprogressiveopacificationofthelens.Theunderlyingmechanismsofdiabeticcataractremainunclear.ThisstudyaimedtoinvestigatetheroleoftheNotchsignalingpathwayinhighglucose-inducedapoptosisofhumanlensepithelialcells(HLECs),focusingontheinvolvementofP53andBAXproteins.
Introduction:
Diabeticcataractisamajorcauseofvisualimpairment,oftenoccurringinpatientswithpoorlycontrolleddiabetes.Highglucoselevelshavebeenimplicatedasamajorcontributortothedevelopmentofdiabeticcataract,leadingtooxidativestressandcelldeathinlensepithelialcells.Notchsignalinghasemergedasacriticalpathwayregulatingcellfatedecisionsandapoptosisinvariouscellularcontexts.However,itsroleinhighglucose-inducedapoptosisinHLECsremainslargelyunexplored.ThisstudyaimstobridgethisknowledgegapbyinvestigatingtheinvolvementofP53andBAXproteinsinNotchsignaling-mediatedapoptosisinHLECsunderhighglucoseconditions.
Methods:
1.Cellculture:Humanlensepithelialcells(HLECs)willbeculturedanddividedintocontrolandhighglucosegroups.
2.Highglucosetreatment:HLECsinthehighglucosegroupwillbetreatedwithahighglucosemediumtomimicthediabeticcondition.
3.Notchsignalingmodulation:HLECsinthehighglucosegroupwillbetreatedwithNotchsignalinginhibitorsoractivatorstoassesstheimpactonapoptosis.
4.Detectionofapoptosis:ApoptosiswillbeassessedusingAnnexinV/propidiumiodidestainingandflowcytometry.
5.Quantitativereal-timepolymerasechainreaction(qRT-PCR):TheexpressionlevelsofgenesrelatedtoNotchsignaling,P53,andBAXwillbedetermined.
6.Westernblotanalysis:ProteinexpressionlevelsofNotchsignalingcomponents,P53,andBAXwillbeevaluated.
7.Statisticalanalysis:Datawillbeanalyzedusingappropriatestatisticalmethodstodeterminesignificantdifferencesbetweengroups.
Results:
OurpreliminaryfindingsdemonstratedthathighglucosetreatmentincreasedHLECapoptosiscomparedtothec