简介：Theirretrievablefateofneuronsdominatedtheneurosciencerhetoricforthefirsthalfofthiscentury,apositionthatwasfiercelycontestedandrecentlydebunkedbyextensivestudiescarriedoutinthefieldofneuroregenerationresearch.Theturningpointcameintheyear1928,whenRamonY.Cajal’s(Lobato,2008)worksuggestedthattheregenerativecapacityof

简介：BACKGROUND:Previousresearchhasrevealedthatsomatostatincaninduceepilepsy,andthatthelevelsofneuropeptideYmayincreaseandbecomemoreactiveinbrainareaswithepilepticseizures.OBJECTIVE:ToobservetheeffectofGanodermalucidumsporepowderontheneuropeptideYandsomatostatincontentinthecerebralcortexandhippocampalregionsofseizureratsinducedbypentylenetetrazol(PTZ).Furthermore,toverifyanyeffectofGanodermalucidumsporepowderoninhibitionofepilepticseizures.DESIGN,TIMEANDSETTING:ArandomizedgroupanimalstudywasperformedinAugust2007intheSchoolofBasicMedicalSciences,JiamusiUniversity(Jiamusi,Heilongjiang,China).MATERIALS:Thirtyhealthy,male,Wistarrats,aged12weeksandweighing180–220g,weretakenastheexperimentalanimals.PTZ(SigmaCompany,UnitedStates)wasusedtoinduceepilepsy.Ganodermalucidumspores(Leyss,exFrvariety)werepurchasedfromJiamusiCityWildGrowingCaseoftheGanodermaLucidum(China).Rabbitanti-somatostatinantibodiesandsecondaryantibodieswerepurchasedfromWuhanBosterCompany(China).NeuropeptideYradioimmunoassaykitwaspurchasedfromBeijingFuruiBiotechnologyCompany(China).METHODS:Thirtyratswererandomlydividedintothreegroups:acontrolgroup,anepilepsymodelgroupandaGanodermalucidumspore-treatedgroup.Eachgroupcontained10animals.RatsintheepilepsymodelgroupweretreatedwithintraperitonealinjectionsofPTZandgastricperfusionofphysiologicsaline.IntheGanodermalucidumspore-treatedgroup,intraperitonealinjectionofPTZandgastricperfusionofGanodermalucidumsporepowderwereadministered.Theblankcontrolgroupwasonlyadministeredwiththephysiologicalsalinebyintraperitonealinjectionandgastricperfusion.MAINOUTCOMEMEASURES:ImmunohistochemicalstainingandradioimmunoassaymethodswereusedtoobservethechangesofsomatostatinandneuropeptideYcontentinbraintissueofepilepticrats,aswellasthemorphologyofneurons

简介：ThisstudysoughttoidentifydifferentiallyexpressedproteinsinSH-SY5Ycellstreatedwithvalproicacid,usingtwo-dimensionaldifferencegelelectrophoresisanalysis.Threeproteinswereunambi-guouslyidentified:theeukaryotictranslationinitiationfactor4Aisoform1andATP6V1B2proteinweredownregulated,whiletheheterogeneousnuclearribonucleoproteinKwasupregulated.Moreover,allthreeproteinsareassociatedwithalteredexpressionduetooxidativestress.Ma-trix-assistedlaserdesorption/ionization-timeofflightmassspectrometryandproteinimmunoblottingassayconfirmedthedifferentialexpressionofeukaryotictranslationinitiationfactor4Aisoform1.Theresultsindicatethatvalproicacidexertsanantioxidationeffectbyregulatingtheexpressionofeukaryotictranslationinitiationfactor4Aisoform1.

简介：Freeradicalsinducedbytraumaticbraininjuryhavedeleteriouseffectsonthefunctionandantioxidantvitaminlevelsofseveralorgansystemsincludingthebrain.Melatoninpossessesantioxidanteffectonthebrainbymaintainingantioxidantenzymeandvitaminlevels.Weinvestigatedtheeffectsofmelatoninonantioxidantabilityinthecerebralcortexandbloodoftraumaticbraininjuryrats.Resultsshowedthatthecerebralcortexβ-carotene,vitaminC,vitaminE,reducedglutathione,anderythrocytereducedglutathionelevels,andplasmavitaminClevelweredecreasedbytraumaticbraininjurywhereastheywereincreasedfollowingmelatonintreatment.Inconclusion,melatoninseemstohaveprotectiveeffectsontraumaticbraininjury-inducedcerebralcortexandbloodtoxicitybyinhibitingfreeradicalformationandsupportingantioxidantvitaminredoxsystem.

简介：Mitochondriaplayanimportantroleinneuronalapoptosiscausedbycerebralischemia,andtheroleismediatedbytheexpressionofmitochondrialproteins.Thisstudyinvestigatedtheinvolvementofmitochondrialproteinsinhippocampalcellapoptosisaftertransientcerebralischemia-reperfusioninjuryinagedratsusingacomparativeproteomicsstrategy.Ourexperimentalresultsshowthattheagedratbrainissensitivetoischemia-reperfusioninjuryandthattransientischemialedtocellapoptosisinthehippocampusandchangesinmemoryandcognitionofagedrats.Differentialproteomicsanalysissuggestedthatthisphenomenonmaybemediatedbymitochondrialproteinsassociatedwithenergymetabolismandapoptosisinagedrats.Thisstudyprovidespotentialdrugtargetsforthetreatmentoftransientcerebralischemia-reperfusioninjury.

简介：BACKGROUND:ItisknownthatacupuncturetherapycandecreaseplasmaneuropeptideY(NPY)levelsinpatientswithcerebralinfarction,butdifferenttypesofacupuncturetherapyusedinvariousstagesofcerebralinfarctionhavenotbeenevaluated.OBJECTIVE:Toexploretheeffectofacupuncturetherapyonresuscitation(XingnaoKaiqiao)andplasmaNPYlevelsinpatientswithveryearlystageacutecerebralinfarction.DESIGN,TIMEANDSETTING:Thiscase-controlledstudywasperformedattheAffiliatedHospitaloftheMedicalCollegeoftheChinesePeople'sArmedPoliceForcebetweenSeptember2004andOctober2005.PARTICIPANTS:Sixtypatientswithacutecerebralinfarctionof≤6hourswereusedinthisstudy.Patientswererandomlydividedintoanacupuncturetherapygroup(n=30)andaroutinetreatmentgroup(n=30).Another30healthysubjectswereusedasthecontrolgroup.METHODS:TheacupuncturetherapyofXingnaoKaiqiaousedintheacupuncturetherapygroupwasbasedonroutinewesternmedicaltreatmentandwasperformedatbilateralNeiguan(PC6)usingthetwirling,reinforcing-reducingmethod,Renzhong(DU26)usingheavybird-peckingneedling,Sanyinjiao(SP6)usingreinforcingandreducingbyliftingandthrustingtheneedle,Jiquan(HT1),Weizhong(BL40)andChize(LU5)usingreinforcingandreducingbyliftingandthrustingtheneedle.Theacupuncturelastedfor14days.Patientsintheroutinetreatmentgroupunderwentroutinemedicaltreatmentandnointerventionwasgiventosubjectsinthecontrolgroup.MAINOUTCOMEMEASURES:A4mLvenousbloodsamplewasobtainedatdifferenttimepoints,i.e.,immediatelyafterhospitalization,thenextmorning,7and14daysaftertreatment,tomeasureplasmaNPYlevelspre-andpost-treatmentusingtheradio-immunitymethod.RESULTS:TheplasmaNPYlevelsweresignificantlyhigherinboththeroutinetreatmentgroupandtheacupuncturetherapygroupthaninthecontrolgrouppre-andpost-treatment(P<0.01).Inparticular,theplasmaNPYlevelsinboththeacupuncturetherapygroupa