简介：目的：探讨褪黑素对过氧化氢诱导晶状体上皮细胞氧化损伤的保护作用。方法：晶状体上皮细胞传代培养后,分别加入不同浓度褪黑素预处理12h后,加入100μmol/LH2O2继续孵育24h,MTT比色法检测褪黑素对H2O2诱导的晶状体上皮细胞活力的影响,流式细胞仪检测细胞凋亡率,比色法检测凋亡相关因子Caspase-3及Caspase-9的活性。结果：MTT结果显示褪黑素对晶状体上皮细胞活性无影响,该药物可以抑制过氧化氢诱导的细胞活性的下降,流式细胞计数结果显示褪黑素可以抑制过氧化氢诱导的细胞凋亡,此外,褪黑素还可以减少过氧化氢所致晶状体上皮细胞内Caspase-3及Caspase-9的活性,并且,伴随褪黑素作用时间的延长其活性呈下降趋势。结论：褪黑素可以明显抑制过氧化氢诱导的晶状体上皮细胞的凋亡,从而为寻求有效的防治白内障药物提供可靠的实验依据。

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

简介：AIM:Topresenttheoutcomeofmodifiedgridlaserphotocoagulation(GLP)indiffusediabeticmacularedema(DDME)ineyeswithoutextrafovealand/orvitreofovealtraction.METHODS:InclusioncriteriafortheretrospectivestudywereDDMEeyesofpatientswithtypeⅡdiabetesmellitusthathad≥4monthsoffollow-upfollowingGLP.Onlyoneeyeperpatientwasanalyzed.Using3-Dspectral-domainopticalcoherencetomography(3-DSDOCT),eyesthathadeitherextrafovealorvitreofovealtraction,orhadbeenpreviouslytreatedbyanintravitrealmedication(s)wereexcluded.TreatedDDMEeyesweredividedinto4groups:A)'Classic'DDMEthatinvolvedthecentralmacula;B)edemadidnotinvolvethemacularcenter;C)eyesassociatedwithcentralepiretinalmembrane(ERM);D)DDMEthatwasassociatedwithmacularcapillarydropout≥2disc-diameter(DD).RESULTS:GLPoutcomein35DDMEeyesafter4-24(mean,13.1±6.9)monthswasasfollows:GroupA)18eyeswith'classic'DDME.Followingoneor2(mean,1.2)GLPtreatments,best-correctedvisualacuity(BCVA)improvedby1-2Snellenlinesin44.4%(8/18)ofeyes,andworsenedby1linein11.1%(2/18).Centralmacularthickness(CMT)improvedby7%-49%(mean,26.6%)in77.8%(14/18)ofeyes.CausesofCMTworsening(n=4)werecommonlyexplainable,predominantly(n=3)associatedwithemergenceofextrafovealtraction,5-9monthspost-GLP.GroupB)GLP(s)inDDMEthatdidnotinvolvethemacularcenter(n=6)resultedinimprovedBCVAby1-2linesin2eyes.However,thecentralmaculabecameinvolvedintheedemaprocessaftertheGLPin3(50%)eyes,associatedwithanemergenceofextrafovealtractioninoneoftheseeyes4monthsfollowingtheGLP.GroupC)GLPfailedinall5eyesassociatedwithcentralERM.GroupD)GLPwasofpartialbenefitin2of6treatedeyeswithmacularcapillarydropout≥2DD.CONCLUSION:EyeswithDDMEthatinvolvedthemacularcenterwerefoundtoachievefavourableoutcomesafterGLP(s)duringmid-termfollow-up,unlesscomplicatedpre-GLPorpost-GLPbyvltreoretinalinterfaceabnormalities,oftenextrafovealtra