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1、徐矧醫(yī)學(xué)院碩士學(xué)位論文PartI.TheEffectsofIsofluranePrecOnditioningagainstCerebralIschemicReperfusionInjuryandonDistributionofPKCTinRatsAbstractobjectiveToinvestigatetheprotectiveeffectofisofluranepreconditioningagainstfocalcerebralischemia—reperfusioninjuryinratsandchangesofPKCT
2、inthefrontallobecerebralcortex.MethodsTwenty-fourmaleSDratsweighing250—3009wererandomlyallocatedintosham-operated,ischemia-reperfusion,isofluranepreconditioninggroups(藏一8).Middlecerebralarteryocclusion(MCAO)wasperformedbysurgicalexposureofcommon,internalandexternalca
3、rotidarteriesthroughalongJitudinalincisionintheneck.AnyZonfilament(0.25—0.28mmindiameter)withroundedendwasinsertedinternalcarotidarteryandthreadedcraniallyuntilresistancewasfelt.Thedepthofinsertionwasabout17—18ram.After2hoursofischemia,theratsinischemic-reperfusiongr
4、oupwerekilledat24hourofreperfusion。Carotidarteriesoftheratsinsham-operationgroupwereexposedbutthedepthofinsertionwaslessthan9mm.Ratsinisofluranepreconditioninggroupinhaled1.5%isofluranelhourandahalfbeforeMCAOwasperformedandtheinhalationlastfor1hour.After24hoursreperf
5、usion,neurologicaldeficitoftheanimalswasassessedbyZeaLonga’sscoringsystem(O=nodeficit,4=unabletowalkandunconscious).Theratswerethenkilled,infarctsizewasdeterminatedbyTTCstaining,andtheexpressionofPKC7infrontallobecerebralcortexWasevaluatedusingimmunofluorescence。Resu
6、ltsNeurologicaldeficitandinfarctsizeinischemia—reperfusionandisofluranepreconditioninggroupsweresignificantlyhigherthanthoseinsham—operatedgroup(P<0.oi).111eamountofPKCTreducedinischemia—reperfusiongroup,butincreasedinisofluranepreconditioninggroupcomparedwithsham-op
7、erationgroup.AndthePKCTdistributedmainlyOVercellmembrane.Comparedwithischemia-reperfusiongroup,neurologicaldeficitandinfarctsizeoftheratssignificantlyreducedinisofluranepreconditioninggroup,buttheexpressionofPKCy4徐州醫(yī)學(xué)院碩士學(xué)位論文1ncreasedinfrontallobecerebralcortex【P8、).ConclusionIsofluranepreconditioningiscapableofinducingneuroprotectionagainstfocalcerebralischemia-reperfusioninjury,andtheprotect