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1、OriginalArticleASNNeuroIntranasalAdministrationofInterferonSeptember-October2016:114!TheAuthor(s)2016DOI:10.1177/1759091416670492BetaAttenuatesNeuronalApoptosisviaasn.sagepub.comtheJAK1/STAT3/BCL-2PathwayinaRatModelofNeonatalHypoxic-IschemicEncephalopathy11111BrandonJ.Dixon,DiChen,YangZhang,J
2、erryFlores,JayMalaguit,11,21DerekNowrangi,JohnH.Zhang,andJipingTangAbstractNeonatalhypoxic-ischemicencephalopathy(HIE)isaninjurythatoftenleadstodetrimentalneurologicaldeficits.Currently,therearenoestablishedtherapiesforHIEanditiscriticaltodeveloptreatmentsthatprovideprotectionafterHIE.Theobje
3、ctiveofthisstudywastoinvestigatetheabilityofinterferonbeta(IFNb)toprovideneuroprotectionandreduceapoptosisafterHIE.PostnatalDay10ratpupsweresubjectedtounilateralcarotidarteryligationfollowedby2.5hrofexposuretohypoxia(8%O2).IntranasaladministrationofhumanrecombinantIFNboccurred2hrafterHIEandin
4、farctvolume,bodyweight,neurobehavioraltests,histology,immunohistochemistry,brainwatercontent,bloodbrainbarrierpermeability,enzyme-linkedimmunosorbentassay,andWesternblotwereallusedtoevaluatevariousparameters.TheresultsshowedthatbothIFNbandtheType1interferonreceptorexpressiondecreasesafterHIE.
5、IntranasaladministrationofhumanrecombinantIFNbwasabletobedetectedinthecentralnervoussystemandwasabletoreducebraininfarctionvolumesandimproveneurologicalbehaviortests24hrafterHIE.Westernblotanalysisalsorevealedthathumanrecom-binantIFNbtreatmentstimulatedStat3andBcl-2expressionleadingtoadecreas
6、eincleavedcaspase-3expressionafterHIE.PositiveFluoro-JadeCstainingalsodemonstratedthatIFNbtreatmentwasabletodecreaseneuronalapoptosis.Furthermore,thebeneficialeffectsofIFNbtreatmentwerereversedwhenaStat3inhibitorwasapplied.Alsoanintraper-itonealadministrationofhumanrecombinantIFNbintothesyste
7、miccompartmentwasunabletoconferthesameprotectiveeffectsasintranasalIFNbtreatment.Keywordsanti-apoptosis,infarctvolume,interferonbeta,intranasaladministration,neonatalstroke,neuronaldegenerationReceivedApril1,2016;ReceivedrevisedJuly25,2016;Ac
