简介:AIM:ToinvestigatetheregulationofEaf2proteininmouselenscellsapoptosisinducedbyultraviolet(UV)radiation.METHODS:AneyeofEaf2geneknockoutmiceornormalcontrolmicewasexposedtoUVradiation,andtheotheronewasnon-exposed.AlloflenseswereanalyzedbyTUNELandcaspase3activityassaystodeterminethedifferenceoftheapoptosisinducedbyUVradiation.Inaddition,exposedandnon-exposedlenseswereanalyzedbyquantifiedp53expressionandreal-timereversetranscription-polymerasechainreaction(RT-PCR)ofBax,Bid,Apaf-1,PumaandNoxa,tocompareEaf2geneknockoutmiceandnormalcontrolmice.RESULTS:UVradiationcausedapoptosisoflenscellsinnormalcontrolmiceandEaf2knockoutmice.Activityofcaspase3wassignificantlyhigherinnormalcontrolmicethanEaf2knockoutmice.Expressionofp53proteinwassignificantlyhigherinlensesexposedtoUVradiationthannonexposedlenses,butwassimilarbetweenEaf2geneknockoutmiceandnormalcontrolmiceinthesameUVcondition.AfterexposingtoUVradiation,theanalysisofreal-timeRT-PCRdemonstratedthatmRNAlevelsofPumaandNoxaweresignificantlyhigherinlensesofnormalcontrolmicethanEaf2geneknockoutmice,andthatmRNAlevelsofBax,BidandApaf-1werenotsignificantlydifferentbetweengeneknockoutmiceandnormalcontrolmice.CONCLUSION:Eaf2increaseslenscellsapoptosisinducedbyultravioletradiation.AndEaf2up-regulatesexpressionofthePumaandtheNoxatoactonlenscellsapoptosisafterUVradiation.
简介:AIM:Toexploretheeffectofsaturatedhydrogensalineonbluelight-inducedretinaldamageinrats.·METHODS:Theretinaldamageofratswasinducedbybluelightexposurefor6hoursandexamined8hours,16hoursand24hoursaftertheexposure.OnehundredfemaleSprague-Dawleyratswererandomlydividedintofourgroups.Group1included30ratsreceivedlightexposurewithoutanyothertreatment.Group2included30ratsreceivedlightexposurewithintraperitonealinjectionofnormalsaline.Group3included30ratsreceivedlightexposurewithintraperitonealinjectionofsaturatedhydrogensaline.AndGroup4includedtheother10ratswhichdidnotreceiveanytreatment.Theamountofintraperitonealinjectionofsaturatedhydrogensalineandnormalsalinewascalculatedintheratioof1ml/100gofratweight.SpecimenswerecollectedandprocessedbyH-Estaining,ultrastructureobservation,biochemicalmeasurement.Morphologicalchangeswereobservedbylightmicroscopeandtransmissionelectronmicroscope(TEM)andtheretinalouternuclearlayer(ONL)thicknesswasmeasuredbyIPP6.0,whilethemalondialdehyde(MDA)wasmeasuredbycolorimetricdeterminationat532nm.·RESULTS:AlthoughthestructureofretinainGroup1andGroup2wasinjuredheavily,theinjuryinGroup3wasmild.ThedifferencesbetweenGroup1andGroup2werenotsignificant.ComparedwiththeratsinGroup1andGroup2,theonesinGroup3hadmoreclearlydemarcatedretinastructureandmoreorderedcellsbylightmicroscopeandTEMobservation.TheONLthicknesses(400times)offourgroupsateachtimepointexceptbetweenGroup1andGroup2weresignificantlydifferent(P<0.05).ThethicknessesoftheONLinGroup1atthreetimepointswere30.41±4.04μm,26.11±2.82μmand20.63±1.06μm,inGroup2were31.62±4.54μm,25.08±3.63μmand19.07±3.86μm,inGroup3were29.75±3.62μm,28.83±1.97μmand27.61±1.83μm.InGroup4themeanofthethicknesswas37.35±1.37μm.Astimewentby,thedamageg