Postconditioning with Inhaled Carbon Monoxide Counteracts Apoptosis and Neuroinflammation in the Ischemic Rat Retina 英文参考文献.docVIP

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Postconditioning with Inhaled Carbon Monoxide Counteracts Apoptosis and Neuroinflammation in the Ischemic Rat Retina 英文参考文献.doc

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Postconditioning with Inhaled Carbon Monoxide Counteracts Apoptosis and Neuroinflammation in the Ischemic Rat Retina 英文参考文献

PostconditioningwithInhaledCarbonMonoxide CounteractsApoptosisandNeuroinflammationinthe IschemicRatRetina NilsSchallner1*,MatthiasFuchs1,ChristianI.Schwer1,TorstenLoop1,HartmutBuerkle1 ,Wolf AlexanderLagre`ze2,ChristianvanOterendorp2,JuliaBiermann2.,UlrichGoebel1. 1DepartmentofAnesthesiologyandCriticalCareMedicine,UniversityMedicalCenterFreiburgimBreisgau,Germany,2UniversityEyeHospital,UniversityMedicalCenter, Freiburg,Germany Abstract Purpose:Ischemiaandreperfusioninjury(I/R)ofneuronalstructuresandorgansisassociatedwithincreasedmorbidityand mortality due to neuronal cell death. We hypothesized that inhalation of carbon monoxide (CO) after I/R injury (‘postconditioning’)wouldprotectretinalganglioncells(RGC). Methods:RetinalI/RinjurywasperformedinSprague-Dawleyrats(n=8)byincreasingocularpressure(120mmHg,1h). RatsinhaledroomairorCO(250ppm)for1himmediatelyfollowingischemiaorwith1.5and3hlatency.Retinaltissuewas harvestedtoanalyzeBcl-2,Bax,Caspase-3,HO-1expressionandphosphorylationofthenucleartranscriptionfactor(NF)-kB, p38andERK-1/2MAPK.NF-kBactivationwasdeterminedandinhibitionofERK-1/2wasperformedusingPD98059(2mg/ kg). Densities of fluorogold prelabeled RGC were analyzed 7 days after injury. Microglia, macrophage and Mu¨ller cell activationandproliferationwereevaluatedbyIba-1,GFAPandKi-67staining. Results:InhalationofCOafterI/RinhibitedBaxandCaspase-3expression(Bax:1.960.3vs.1.460.2,p=0.028;caspase-3: 2.060.2 vs. 1.560.1, p=0.007; mean6S.D., fold induction at 12h), while expression of Bcl-2 was induced (1.260.2 vs. 1.660.2, p=0.001; mean6S.D., fold induction at 12h). CO postconditioning suppressed retinal p38 phosphorylation (p=0.023 at 24h) and induced the phosphorylation of ERK-1/2 (p,0.001 at 24h). CO postconditioning inhibited the expressionofHO-1.TheactivationofNF-kB,microgliaandMu¨llercellswaspotentlyinhibitedbyCOaswellasimmigration ofproliferativemicrogliaandmacrophagesintotheretina.COprotectedI/R-injuredRGCwithatherapeuticwindowatleast upto3h(n=8;RGC/mm2;mean