简介：AIM:ExcessivedissolveofcornealtissueinducedbyMMPswhichwereactivatedbycytokinsandchemokineswillleadtocornealulcer.ThemolecularmechanismofLipoxinA4(LXA4)oncornealcollagendegradationinthreedimensionswasinvestigated.·METHODS:Rabbitcornealfibroblastswereharvestedandsuspendedinserum-freeMEM.TypeIcollagen,DMEM,collagenreconstitutionbufferandcornealfibroblastsuspensionweremixedonice.Theresultantmixturesolidifiedinanincubator,afterwhichtestreagentsandplasminogenwasoverlaidandthecultureswerereturnedtotheincubator.Thesupernatantsfromcollagengelincubationswerecollectedandtheamountofhydroxyprolineinthehydrolysatewasmeasured.ImmunoblotanalysisofMMP-1,-3andTMMP-1,-2wasperformed.MMP-2,-9wasdetectedbythemethodofGelatinzymography.Cytotoxicityassaywasmeasured.RESULTS:LXA4inhibitedcornealcollagendegradationinadoseandtimemanner.LXA4inhibitedtheIL-1βinducedincreasesinthepro-MMP-1,-2,-3,-9andactiveMMP-1,-2,-3,-9inaconcentrationdependentmanner.LXA4alsoinhibitedtheIL-1βinducedincreasesinTIMP-1,-2.CONCLUSION:Asapotentanti-inflammationreagent,LXA4caninhibitcornealcollagendegradationinducedbyIL-1βincornealfibroblaststhusinhibitingcornealdissolvingpathologyprocess.

简介：近视眼的发病与多种因素相关,其中最主要的是遗传和环境因素.大量的近视相关研究提示近视的发生是在异常视觉信息的作用下,视网膜、脉络膜内多种神经递质和生长因子的表达发生改变,通过一系列信号传导过程引起巩膜重塑、眼轴延长而成.多种细胞因子通过NMDAR-1/NO-cGMP、TGF-β1/Smad3、JAK-Stat3等信号通路调控近视的形成与发展.本文就影响近视形成的几个主要信号传导通路的研究进展做一综述.

简介：AIM:ToinvestigatetheeffectofintravitrealinjectionofDL-alpha-aminoadipicacid(DL-α-AAA)onocularrefractivestateandretinaldopamine,transforminggrowthfactor-β2(TGFβ2),vasoactiveintestinalpolypeptide(VIP)inguineapigform-deprivedmyopia.METHODS:Four-week-oldpigmentedguineapigswererandomlyassignedto4groups:normalcontrol,deprivation,deprivationplusDL-α-AAA,deprivationplussaline.Formdeprivationwasinducedwiththeself-madetranslucenteyeshields,andlastedfor14days.8μgDL-α-AAAwasinjectedintothevitreouschamberofdeprivedeyes.Thecornealradiusofcurvature,refractionandaxiallengthweremeasured.Retinaldopaminecontentwasevaluatedbythehigh-performanceliquidchromatographywithelectrochemicaldetection,andTGFβ2andVIPproteinweredetectedbyWesternblotting.RESULTS:Fourteendaysofeyeocclusioncausedtheaxiallengthtoelongateandbecomemyopicintheform-deprivedeyes,withthedecreaseofretinaldopamineandtheincreaseofTGFβ2andvasoactiveintestinalpolypeptide(VIP)protein.IntravitrealinjectionofDL-α-AAAcouldinhibitthemyopicshiftfrom(-3.65±1.06)Dto(-1.48±0.63)D,P<0.01duetogogglesoccludingandcausethedecreaseofretinalTGFβ2proteininthedeprivedeyes.However,intravitrealinjectionofDL-α-AAAhadnosignificanteffectonretinaldopamineandVIPproteinindeprivedeyes.RetinalTGFβ2proteincorrelatedhighlywiththeocularrefraction(y=-3.34+0.31/x,F=74.75,P<0.001)andaxiallength(y=8.39-0.02/x,F=48.32,P<0.001)indifferenttreatmentgroups.·CONCLUSION:IntravitrealinjectionofDL-α-AAAiseffectivelyabletosuppressthedevelopmentofformdeprivationmyopia,whichmaybeassociatedwithretinalTGFβ2proteininguineapigs.