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1、第三军医大学硕士学位论文NSSNeurologicalseverityscore神经功能缺损评分PBSphosphate-buffersolution磷酸盐缓冲液TTC2,3,5-Triphenyltetrazoliumchloride2,3,5-氯化三苯基四唑氮μgmicrogramme微克2第三军医大学硕士学位论文ProtectiveEffectandItsMechanismofHyperbaricOxygenPreconditioningonPermanentMiddleCerebralArteryOcclusionofMiceAb
2、stractBackgroundandobjectiveCerebrovasculardiseaseisoneofthethreediseaseswithhighestmorbidityaroundtheworld,whiletheincidenceofischemiccerebrovasculardiseaseaccountsformorethan85%ofthetotalincidencerateofcerebralvasculardiseases,whichbringsinaheavysocialandeconomicalburde
3、n.Cerebralischemiaalsocanoccurtothepatientswithotherchronicdiseases.Ithasbeenamajoranddifficulttaskinneurosurgerytoinducethebrain’toleranceonischemicconditionandalleviatethedamagetonervefunctionafterischemia.InourPreliminarystudy,hyperbaricoxygenpreconditioning(HBOP)hasap
4、rotectiveeffectontheanimalsundergoingcerebralischemiaorspinalcordinjury.AdditionallyplentyofliteratureshavereportedthatHBOPcaninduceischemictoleranceintheorganssuchasheart,liver,kidney,spinalcordandbrain,whereasitsunderlyingmechanismsremainunclear.TheP2X7receptorisamember
5、ofthepurinergicP2XfamilyofATP-gatedionchannel,anddistributeswildlyinbrain.P2X7receptorisoneoftheupstreamregulatorysitesintheprocessofischemicbraininjury.Afterischemia,activationofP2X7receptorcanleadtothedeathofoligodendrocytesaswellasdamageofmyelinandwhitematter.meanwhile
6、theactivationofP2X7receptorwillinvokethemicrogliasandastrocytesandleadtothereleaseofinflammatoryfactorssuchasIL-1β,TNF-a,etc,whichwouldcausenecrosisandapoptosisofnervecell.Furthermore,Aquaporin4(AQP4)isthemostaboundantwaterchannelproteininbrain,playinganimportantroleinmai
7、ntainingthehomeostasisinbrain.Aftercerebralischemia,AQP4participatesinthegenesisanddevelopmentofearlycytotoxicbrainedema.Besides,itplaysaroleinthestabilityofinternalenvironmentandneuralsignaltransductionbyregulatingtheastrocytefunction.3第三军医大学硕士学位论文Ourpreviousresearchhads
8、howedthatHBOPiscapabletoregulatetheexpressionofP2X7receptorafterspinalcordinjury,studieshaveshow
