简介：AIM:ToinvestigatetheinterferingeffectofY-27632,aROCK-Iselectiveinhibitor,onthesignaltransductionpathwayoftransforminggrowthfactor-β1(TGF-β1)inocularTenoncapsulefibroblasts(OTFS)invitro.METHODS:AfterOTFSfrompassages4to6invitrowereinducedbyTGF-β1andthentreatedbyY-27632,thechangesoftheOTFScellcycleswereanalyzedviaflowcytometry,andtheproteinsexpressionoftheα-smoothmuscularactin(α-SMA),connectivetissuegrowthfactor(CTGF),collagenIwerecalculatedbyWesternblot.AfterOTFStreatedbythedifferentconcentrationsofY-27632,theexpressionlevelsoftheα-SMA,CTGFandcollagenImRNAwereassayedbyRT-PCR.RESULTS:Y-27632hadnomarkedlyeffectontheOTFScellcycles.AftertreatedbyTGF-β1,OTFSinG1periodsignificantlyincreased.ThecellcyclesdistributionbybothTGF-β1andY-27632hadnoremarkabledifferencefromthatincontrolgroup.Y-27632significantlyinhibitedtheproteinsexpressionsofbothα-SMAandCTGF,whiletosomeextentinhibitedthatofcollagenI.TGF-β1significantlypromotedtheproteinsexpressionsofα-SMA,CTGFandcollagenI.AfterOTFStreatedbybothTGF-β1andY-27632,ofα-SMA,theproteinexpressionwassimilarwiththatincontrolgroup(P=0.066>0.05),buttheproteinexpressionofCTGForcollagenI,respectively,wassignificantlydifferentfromthatincontrolgroup(P=0.000<0.01).Thedifferencesofexpressionsoftheα-SMA,CTGFandcollagenImRNAin30,150,750μmol/LY-27632groupwerestatisticallysignificant,comparedwiththoseincontrolgroup,respectively(α-SMA,P=0.002,0.000,0.000;CTGF,P=0.014,0.002,0.001;collagenI,P=0.003,0.002,0.000).CONCLUSION:BlockingtheRho/ROCKsignalingpathwaybyusingofY-27632couldinhibitthecellularproliferationandtheexpressionofbothCTGFandα-SMAwhateverOTFSinducedbyTGF-β1ornot.Y-27632suppressedtheexpressionofcollagenImRNAwithoutinduction.

简介：AIM:Toinvestigatethelevelsofserumsolubleintercellularadhesionmolecules-1(sICAM-1)andneutrophilicexpressionofCD18inpatientswithvariousstagesofdiabeticretinopathyandtodeterminetheirdifferentexpressionpatterninthedevelopmentofdiabeticretinopathy(DR).·METHODS:LevelsofserumsICAM-1andCD18onthesurfaceofneutrophileweremeasuredin41DRpatients,theywereclassifiedinthreesubgroupsaccordingtothestageofretinopathyasdeterminedbyfund’sophthalmoscopy;10controlsubjectswerealsostudied.sICAM-1weremeasuredbyenzyme-linkedimmunosorbentassayandCD18byflowcytometry.·RESULTS:TheneutrophilicCD18expressionandserumsICAM-1levelwereallsignificantlyelevatedinalldiabeticsubgroupscomparedtocontrolsubjects(P<0.01).ThedifferencesofCD18andsICAM-1amongthediabeticsubgroupsweresignificantinCD18butnotinsICAM-1.TheprogressionofretinopathywasassociatedwithanincreasebothinCD18andinsICAM-1levelsbysimplecorrelationanalysis(β=0.74,P<0.001;β=0.38,P<0.01,respectively).ButstepwisemultipleregressionanalysisrevealedthatonlyCD18wasindependentdeterminantofretinopathy(β=1.04,P<0.01).·CONCLUSION:OurresultsconfirmthecontributionofendothelialandneutrophilicactivationinthedevelopmentofDRasindicatedbyincreasedlevelsofCD18andsICAM-1.However,adirectimplicationofCD18andICAM-1intheprogressionofDRcanbesupportedonlyintheCD18butnotICAM-1.CD18andICAM-1mayplaydifferentroleinthedevelopmentofdiabeticretinopathy.

简介：·AIM:Toexploretheeffectofimmunizationwithcopolymer-1(COP-1)andretinalstemcells(RSCs)transplantationoninterferon-gamma(IFN-γ)levelsinaratexperimentalglaucomamodel.·METHODS:Anexperimentalglaucomawasinducedbyargonlaserphotocoagulationoftheepiscleralveinsandlimbalplexusintherighteyeofrats.Immediatelyfollowingglaucomainduction,ratswereimmunizedwithCOP-1.RSCswereculturedandtransplantedintravitreallyintotheeyesofglaucomamodelanimals1weekpost-lasertreatment.Sixexperimentalgroupswereused:COP-1/RSC,PBS/RSC,COP-1/PBS,PBS/PBS,glaucomamodelgroup,andanormalcontrolgroup.TheconcentrationofIFN-γinaqueoushumor(AH)andserumwasmeasuredbyenzyme-linkedimmunosorbentassay(ELISA)ineachofthesixgroups.Retinalganglioncell(RGC)survivalwasassessedbyquantifyingapoptosisusingHoechststaining.·RESULTS:ConcentrationsofIFN-γinAHandserumofratsthathadundergoneglaucomainductionwerehigherthanthoseofnon-inducedcontrolrats.TheconcentrationsofIFN-γinAHandserumoftheCOP-1/RSCstreatedgroupweredeterminedtobe2371.9ng/Land710.9ng/L,respectively,whichweresignificantlylowerthanthoseintheothertreatedgroups(P<0.05).Infact,IFN-γlevelsinthedualtreatedgroupwerereducedtobackgroundlevels.TheCOP-1/RSCgrouphadlowernumberofapoptoticRGCsthantheotherthreeexperimentalgroups(P<0.05).·CONCLUSION:ThereducedlevelsofIFN-γinAHandserumoftheCOP-1/RSCgroupmayberelatedtosynergisticeffectsbetweenRSCstransplantationandCOP-1immunemodulation.ItislikelythatthelowerlevelsofIFN-γpreventedRGCsglaucomatousapoptosis.·