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简介：Injurytoaxonsclosetotheneuronalbodiesinthemammaliancentralnervoussystemcausesalargeproportionofparentingneuronstodegenerate.Itisknownthatopticnervetransectionclosetotheeyeinrodentsleadstoalossofabouthalfofretinalganglioncellsin1weekandabout90%in2weeks.Usinglowlevellasertreatmentinthepresentstudy,wedemonstratedthattreatmentwithhelium-neon(660nm)laserwith15mWpowercoulddelayretinalganglioncelldeathafteropticnerveaxotomyinadulthamsters.Theeffectwasmostapparentinthefirstweekwithashortperiodoftreatmenttime(5minutes)inwhich65–66%ofretinalganglioncellssurvivedtheopticnerveaxotomywhereas45–47%ofretinalganglioncellsdidsoinopticnerveaxotomycontrols.Wealsofoundthatsingledoseandearlycommencementoflaserirradiationwereimportantinprotectingretinalganglioncellsfollowingopticnerveaxotomy.Thesefindingsthusconvincinglyshowthatappropriatelasertreatmentmaybeneuroprotectivetoretinalganglioncells.更多还原

简介：Theretinaisamultilayeredtissuethatdevelopsfollowingacentral-to-peripheralgradient.Itsstructurederivesfrommultipotentprecursors,asshownthroughclonalanalysisofretinalcelllineage.Theseprogenitorsgeneratediversecelltypes,controlledbycomplexinfluencesofintrinsicandextrinsicfactors(HatakeyamaandKageyama,2004).Severaltypesofneuronsandonemaingliacellconsti-

简介：Intraperitonealinjectionofrecombinanthumaninterleukin-2(rhIL-2)inhibitsneuronalapoptosisinthechronicocularhypertensionretinalganglioncelllayer.IntravitreousinjectionwasperformedonretinalganglioncellsinaWistarratmodelofchronicallyelevatedintraocularpressuretoobservetheeffectsofLY294002andAG490onretinalganglioncellsurvival,macrophageactivation,andPI3K/AktandJAK/STATactivation.ThenumberofretinalganglioncellsintherhIL-2treatmentgroupwasmuchgreaterthaninthenormalcontrolandphosphate-bufferedsalinegroups.WesternblotanalysisrevealedlowAktandSTAT3proteinexpressionintheretinaafter3-hourintravitreousinjectionsofrhIL-2.However,proteinexpressionwasincreasedat12hours,butdecreasedagainat24hours,withverylowexpressionat96hours.LY294002andAG490,whichareinhibitorsofthePI3K/AktandJAK/STAT3signalpathways,preventedupregulationofAktandSTAT3proteinexpressionintheretina,respectively.IntravitreousinjectionofrhIL-2exhibitedneuroprotectiveeffectsbydecreasingretinalganglioncelllayerdamageinaratmodelofchronicglaucoma.TheseresultssuggestthatintravitrealinjectionofrhIL-2couldinducethePI3K/AktandJAK/STAT3signalingpathwaystoprotectretinalganglioncellsinchronicallyelevatedintraocularpressuremodels.