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:ToidentifythefunctionofST2andexploretheroleofIL-33/ST2signalinginregulatingthepro-allergiccytokineproductioninhumancornealepithelialcells(HCECs).METHODS:HumancornealtissuesandculturedprimaryHCECsweretreatedwithIL-33indifferentconcentrationswithoutorwithdifferentinhibitorstoevaluatetheexpression,locationandsignalingpathwaysofST2inregulatingproductionofpro-allergiccytokineandchemokine.TheexpressionofmRNAwasdeterminedbyreversetranscriptionandrealtimePCR,andproteinproductionwasmeasuredbyenzyme-linkedimmunosorbentassay(ELISA),immunohistochemicalandimmunofluorescentstaining.ST2proteinwasdetectedindonorcornealepithelium,andST2signalwasenhancedbyexposuretoIL-33.·RESULTS:IL-33significantlystimulatedproductionofpro-allergiccytokinesthymicstromallymphopoietin(TSLP)andchemokine(CCL2,CCL20,CCL22)inHCECsatbothmRNAandproteinlevels.Thesestimulatedproductionsofpro-allergicmediatorsbyIL-33wereblockedbyST2antibodyorsolubleST2protein(P<0.05).Interestingly,theIκB-αinhibitorBAY11-7082orNF-κBactivationinhibitorquinazolineblockedNF-κBp65proteinnucleartranslocation,andalsosuppressedtheproductionsofthesepro-allergiccytokinesandchemokineinducedbyIL-33.CONCLUSION:ThesefindingsdemonstratethatIL-33/ST2signalingplaysanimportantroleinregulatingIL-33inducedpro-allergicresponses.IL-33andST2couldbecomenovelmoleculartargetsfortheinterventionofallergicdiseasesinocularsurface.
简介:目的:探讨白内障手术切口大小对矫正角膜原有散光、泪膜稳定性的影响。方法:收集我院2014-07/2016-07接诊的白内障患者92例92眼,随机分为对照组和观察组,各46例46眼。两组均行透明角膜隧道切口白内障乳化超声术联合折叠人工晶状体植入术,对照组为3.0mm透明角膜切口,观察组为1.8mm透明角膜切口。检测术前及术后1d,1wk,1、3mo裸眼视力、角膜散光度、基础泪液分泌(schirmerⅠtest,SⅠt)、泪膜破裂时间(break-uptime,BUT),记录术后1d,1wk,1、3mo术源性散光(surgeryinducedastigmatism,SIA)。结果:两组术后1、3mo裸眼视力与术前比较差异有统计学意义(P〈0.05),但两组手术前后不同时间比较差异无统计学意义(P〉0.05);两组术后1、3mo角膜散光与术前比较无明显变化,差异有统计学意义(P〈0.05),两组手术前后各时间点比较差异无统计学意义(P〉0.05);两组术后1wk,1、3moSIA均不断减小,且观察组术后1d,1wk,1moSIA明显低于对照组,差异有统计学意义(P〈0.05)。两组术后1wkSⅠt、BUT少于术前,差异有统计学意义(P〈0.05),术后1、3mo与术前比较差异无统计学意义(P〉0.05);观察组术后1wkSⅠt、BUT高于对照组,差异有统计学意义(P〈0.05),但术后1、3mo比较,差异无统计学意义(P〉0.05)。结论:与3.0mm标准切口相比,1.8mm透明角膜切口可减少SIA,缩短角膜稳定性恢复时间。