Objective:Toinvestigatetheunderlyingneurobiologicalmechanismoftheprotectiveeffectofelectroacupuncture(EA)duringcerebralischemia-reperfusion(CI-R).Methods:Inthefirstpartofthestudy,15SDratswereevenlyrandomizedintocontrolgroup,CI-R-48hmodelgroupandCI-R-48h+EAgroup.ThecorticalapoptosisandexpressionofBcl-2andBaxproteinsineachgroupweredetectedbyflowcytometer(FCM).Inthesecondpartofthestudy,75SDratswereevenlyrandomizedintocontrol,CI-R-3min,CI-R-3min+EA,CI-R-48handCI-R-48h+EAgroups.Corticalnorepinephrine(NE)concentrationwasdetectedbyfluorescencespectrometer.CI-Rmodelwasestablishedbyocclusionofthebilateralcommoncarotidarteriesandreperfusion.EA(4～16Hz,1～3V)wasappliedafterreperfusionrespectively.Results:Inthefirstpartofthisstudy,resultsindicatedthatthenumberoftheapoptoticneuronsandtheapoptosisrateofCI-R-48hgroupweresignificantlyhigherthanthoseofcontrolgroup;whilecomparisonbetweenCI-R-48h+EAandCI-R-48hgroupsshowedthatthenumberoftheapoptoticneuronsandtheapoptosisrateoftheformergroupweresignificantlylowerthanthoseofthelatergroup(P<0.05).Incomparisonwithcontrolgroup,afterCI-48h,Baxexpressionwasup-regulatedsignificantlyandBcl-2down-regulatedmarkedly(P<0.05).ComparisonbetweenCI-R-48handCI-R-48h+EAgroupindicatedthatBaxexpressionofthelatergroupwassignificantlylowerthanthatoftheformergroup,whileBcl-2expressionofCI-R-48h+EAgroupwassignificantlyhigherthanthatofCI-R-48hgroup(P<0.05),suggestingthatEAcouldreverseCIinducedreactionsofthesetwoindexes.Inthesecondpartofthestudy,incomparisonwithcontrolgroup,NEconcentrationincerebralcortexofCI-R-3mingroupincreasedsignificantly(P<0.05);whileNEcontentofCI-R-3min+EAgroupwassignificantlylowerthanthatofCI-R-3mingroup(P<0.05).NosignificantdifferencewasfoundbetweenCI-R-3mingroupandcontrolgroupincorticalNEl
