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简介：Membranedepolarizationinducesthereleaseoftheserineproteinasetissue-typeplasminogenactivator(tPA)fromthepresynapticterminalofcerebralcorticalneurons.OnceinthesynapticcleftthistPApromotestheexocytosisandsubsequentendocyticretrievalofglutamate-containingsynapticvesicles,andregulatesthepostsynapticresponsetothepresynapticreleaseofglutamate.Indeed,tPAhasabidirectionaleffectonthecompositionofthepostsynapticdensity(PSD)thatdoesnotrequireplasmingenerationorthepresynapticreleaseofglutamate,butvariesaccordingtothebaselinelevelofneuronalactivity.Hence,ininactiveneuronstPAinducesphosphorylationandaccumulationinthePSDoftheCa~(2+)/calmodulin-dependentproteinkinaseIIα(pCaMKIIα),followedbypCaMKIIα-inducedphosphorylationandsynapticrecruitmentofGluR1-containingα-amino-3-hydroxy-5-methyl-4-isoxazolepropionicacid(AMPA)receptors.Incontrast,inactiveneuronswithincreasedlevelsofpCaMKIIαinthePSDtPAinducespCaMKIIαandpGluR1dephosphorylationandtheirsubsequentremovalfromthePSD.TheseeffectsrequireactivesynapticN-methyl-D-aspartate(NMDA)receptorsandcyclin-dependentkinase5(Cdk5)-inducedphosphorylationoftheproteinphosphatase1(PP1)atT320.ThesedataindicatethattPAisahomeostaticregulatorofthepostsynapticresponseofcerebralcorticalneuronstothepresynapticreleaseofglutamateviabidirectionalregulationofthepCaMKIIα/PP1switchinthePSD.

简介：NewZealandrabbitswererandomlydividedintoanischemiagroup(occlusionoftheabdominalaortafor60minutes),anischemia-reperfusiongroup(occlusionoftheabdominalaortafor60minutesfollowedby48hoursofreperfusion)andasham-surgerygroup.Two-dimensionalgelelectrophoresisdetected49differentiallyexpressedproteinsinspinalcordtissuefromtheischemiaandischemia/reperfusiongroupsand23ofthemwereidentifiedbymassspectrometry.Intheischemiagroup,theexpressionofeightproteinswasupregulated,andthatoftheremainingfourproteinswasdownregulated.Intheischemia/reperfusiongroup,theexpressionoffourproteinswasupregulated,andthatoftwoproteinswasdownregulated.Inthesham-surgerygroup,onlyoneproteinwasdetected.Intheischemiaandischemia/reperfusiongroups,fourproteinsoverlappedbetweengroupswiththesamedifferentialexpression,includingthreethatwereupregulatedandonedownregulated.Theseproteinswererelatedtoenergymetabolism,celldefense,inflammatorymechanismandcellsignaling.

简介：Therapiesthatcomplementfreeradicalscavengingareanimportantapproachfortreatingaginginthebrain.Inthepresentstudy,twoformulationsofmoxaconemoxibustionwereappliedatacupointsZusanli(ST36)andXuanzhong(GB39),andatacupointsBaihui(DU20)andGuanyuan(RN4),inD-galactose-inducedsenilemice.TheresultsrevealedthatmoxaconemoxibustionimprovedtotalsuperoxidedismutaseandCu/Zn-superoxidedismutaseactivityinthehomogenatesofthecerebraltissue,aswellasamelioratingdeficitsinneuronalmorphologyandneuronaldensityinthecerebralcortexandhippocampalCA3.Moxaconemoxibustionalsoenhancedlearningandmemoryfunctionsofsenilemice.MoxaconemoxibustionatZusanli,Xuanzhong,BaihuiandGuanyuanacupointscanthusbeusedtocomplementfreeradicalscavengers,withefficacythatisequaltothatofelectroacupunctureatZusanliandXuanzhong,andsuperiortothatofnimodipinetreatment.

简介：BACKGROUND:Alongwithaging,antioxidaseactivitydecreasesandoxygen-derivedfreeradicalsgreatlyaccumulate,resultingincellularsenescence,orevencelldeath.Thisismanifestedbyhypomnesiaanddis-orderedmetabolismoffreeradicals.StudieshavereportedthatLongyanshenpolysaccharideshavethefunc-tionofantioxidationandimprovedbrainmemory.OBJECTIVE:ToobservetheeffectsofLongyanshenpolysaccharidesonfreeradicalmetabolisminbraintissuetoverifytheanti-agingmechanismsinsenescenceaccelerated-prone(SAMP8)mice.DESIGN,TIMEANDSETTING:Therandomized,controlled,biochemicalexperimentwasperformedintheDepartmentofPharmacologyandScientificExperimentalCenterofGuangxiMedicalUniversity(China)fromSeptember2005toJanuary2008.MATERIALS:FortySAMP8micewererandomizedintofourgroups:SAMP8controlgroup,aswellaslow-,mid-,andhigh-dosepolysaccharide,with10miceineachgroup.Tensenescenceaccelerated-resistant-prone(SAMR1)miceservedasthenormalcontrolgroup.Longyanshenpolysaccharides,extractedfromthemedicalplantLongyanshen,weresuppliedbytheDepartmentofPharmacology,GuangxiMedicalUniversity.Superoxidedismutase(SOD),glutathioneperoxidase(GSH-Px),malonaldehyde(MDA),nitricoxide(NO),andtotalproteintestkitwerepurchasedfromNanjingJianchengBioengineeringInstitute(China).METHODS:SAMP8micewereusedtoestablishadementiaanimalmodel.SAMP8andSAMR1controlmicewereadministered30mL/kgsaline.Thelow-,middle-,andhigh-dosepolysaccharidegroupswereadministered45,90,and180mg/kgLongyanshenpolysaccharides,respectively.Eachgroupwastreatedbyin-tragastricadministration,oncedaily,for50continuousdays.MAINOUTCOMEMEASURES:Onehourafterthelastadministration,mousebraintissueswerecollected,andretroorbitalbloodsamplingwasperformed.SpectrophotometrywasusedtomeasureSODandGSH-Pxactivity,aswellasMDAandNOconcentrationinseraandbrainsofSAMP8mice.RESULTS:

简介：Excessivenoise,ototoxicdrugs,infections,autoimmunediseases,andagingcancauselossofspiralganglionneurons,leadingtopermanentsensorineuralhearinglossinmammals.Stemcellshavebeenconfirmedtobeabletodifferentiateintospiralganglionneurons.Littlehasbeenreportedonadiposetissue-derivedstemcells(ADSCs)forrepairofinjuredspiralganglionneurons.Inthisstudy,wehypothesizedthattransplantationofneuralinduced-humanADSCs(NI-hADSCs)canrepairtheinjuredspiralganglionneuronsinguineapigswithneomycin-inducedsensorineuralhearingloss.NI-hADSCswereinducedwithculturemediumcontainingbasicfibroblastgrowthfactorandforskolinandtheninjectedtotheinjuredcochleae.GuineapigsthatreceivedinjectionofHanks’balancedsaltsolutionintothecochleaewereusedascontrols.Hematoxylin-eosinstainingshowedthatat8weeksaftercelltransplantation,thenumberofsurvivingspiralganglionneuronsinthecelltransplantationgroupwassignificantlyincreasedthanthatinthecontrolgroup.Alsoat8weeksaftercelltransplantation,immunohistochemicalstainingshowedthatagreaternumberofNI-hADSCsinthespiralganglionsweredetectedinthecelltransplantationgroupthaninthecontrolgroup,andtheseNI-hADSCsexpressedneuronalmarkersneurofilamentproteinandmicrotubule-associatedprotein2.Within8weeksaftercelltransplantation,theguineapigsinthecelltransplantationgrouphadagraduallydecreasedauditorybrainstemresponsethreshold,whilethoseinthecontrolgrouphadalmostnoresponseto80dBofclicksorpuretoneburst.ThesefindingssuggestthatalargeamountofNI-hADSCsmigratedtothespiralganglions,survivedforaperiodoftime,repairedtheinjuredspiralganglioncells,andtherebycontributedtotherecoveryofsensorineuralhearinglossinguineapigs.

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简介：BACKGROUND:Stellateganglionblock(SGB)playsaprotectiveroleonthebrain,buttheprecisemecha-nismofactionisnotclear.OBJECTIVE:TosimulateSGBbytransectionofthecervicalsympathetictrunk(TCST)andtoinvestigatetheTCSTeffectsonchangesincerebralinfarctvolumeandoxygenfreeradicallevelsinratswithfocalcere-bralischemia/reperfusioninjury.DESIGN,TIMEANDSETTING:AcompleterandomizedcontrolanimalexperimentwasperformedattheInstituteofNeurologicalDiseasesofTaiheHospital,YunyangMedicalCollegefromFebruarytoDecember2005.MATERIALS:Atotalof101healthyWistarrats,weighing280–320g,ofbothgenders,aged17–18weeks,wereusedinthisstudy.2,3,5-triphenyltetrazoliumchloride(TTC)waspurchasedfromChangshaHongyuanBiologicalCompany.Superoxidedismutase(SOD),malondialdehyde(MDA)andnitricoxide(NO)assaykitswereprovidedbyNanjingJianchengBioengineeringInstitute.METHODS:RatswererandomlydividedintoaTCSTgroup,amodelgroupandashamoperationgroup.Successfulmodelswereincludedinthefinalanalysis,withatleast20ratsineachgroup.AfterTCST,ratmodelsoffocalcerebralischemia/reperfusioninjurywereestablishedintheTCSTgroupbyreceivingmiddlecerebralarteryocclusion(MCAO)bytheintraluminalsuturemethodfor2hours,followedby24hoursofreperfusion.Ratmodelsoffocalcerebralischemia/reperfusioninjuryweremadeinthemodelgroup.Ratsintheshamoperationgroupunderwentexperimentalproceduresasforthemodelgroup,threadingdepthof10mm,andmiddlecerebralarterywasnotligated.MAINOUTCOMEMEASURES:BraintissuesectionsoftenratsfromeachgroupwereusedtomeasurecerebralinfarctvolumebyTTCstaining.BraintissuehomogenateofanothertenratsfromeachgroupwasusedtodetectSODactivities,MDAcontentsandNOlevels.Ratneurologicalfunctionwasassessedbyneu-robehavioralmeasures.RESULTS:CerebralinfarctvolumewasbiggerinthemodelgroupthanintheTCSTgr

简介：BACKGROUND:Highincidenceofstrokeatinterchangeperiodofautumnandwinterwasdemonstratedbyepidemiologicalsurvey,andthespecificcausesshouldbefurtherinvestigated.OBJECTIVE:Toinvestigatetheinfluenceofartificialcoldexposureontheincidenceofstrokeinrenovascularhypertensiverats(RHR),andanalyzetheassociationwithbloodpressureandcold-inducibleRNAbindingprotein(CIRP)mRNAexpressioninbraintissue.DESIGN:Acompletelyrandomizedgroupingdesign,arandomizedcontrolanimaltrial.SETTINGS:LabofNeurology,theFirstAffiliatedHospitalofSunYat-senUniversity;DepartmentofChemistry,OpenlaboratoryofChemicalBiology,InstituteofMolecularTechnologyforDrugDiscoveryandSynthesis,UniversityofHongKong.MATERIALS:MaleSDrats(n=460),weighing80-100gwereobtainedfromGuangdongProvinceHealthAnimalUnit.AmodifiedRXZ-300Aintelligentartificialclimatecabinet(NingboJiangnanInstrumentCo.,Ltd.,China).METHODS:TheexperimentwereprocessedintheLabofNeurology,theFirstAffiliatedHospitalofSunYat-senUniversityandtheOpenLaboratoryofChemicalBiology,InstituteofMolecularTechnologyforDrugDiscoveryandSynthesis,UniversityofHongKongfromOctober2004toNovember2005.Rats(n=400)wereoperatedtoestablish2-kidney2-clipRHRmodelasdescribedpreviously.Thesham-operatedrats(n=60)servedasnormotensivecontrols.Eightweekslater,300ofRHRwererandomlyselectedaccordingtotheirsystolicbloodpressure(SBP)anddividedinto3sub-groups(n=100pergroup):mildhypertensivegroup(SBPof160-200mmHg),moderatehypertensivegroup(SBPof200-220mmHg)andseverehypertensivegroup(SBP>220mmHg).Eachgroupwasfurtherdividedintotwogroups(n=50)underACEandnon-ACE.Normalsham-operatedSDrats(n=60),SBP<140mmHg,wererandomlydividedintotwogroups:Sham-operatedcontrolgroup(n=30)underACEandnon-ACE.ToestablishtheACEandnon-ACEtreatment,ratswerehousedindividuallyinartifici