简介：BACKGROUND:Culturesfrommultipleportionsofumbilicalcordbloodmesenchymalstemcellshavebeenshowntoundergomorerapidproliferationandattachmentthansingleportions.OBJECTIVE:Toobservegrowthofbasicfibroblastgrowthfactor(bFGF)-inducedculturesofhumanamnion-derivedmesenchymalstemcells(AMSCs)anddifferentiationintoneuronal-likecells.DESIGN,TIMEANDSETTING:Comparativeobservation.ThestudywasperformedattheLaboratoryofMicrobiologyandImmunology,BasicMedicalSchoolofZhengzhouUniversityfromJanuarytoMay2008.METHODS:Amniafromfull-term,uterine-incisiondeliveryweredonatedby12healthywomen.AMSCswereobtainedbycellseparationandculturetechniques,andwerepassagedandinducedbybFGF.Fromthethirdpassage,atotalof1mLAMSCs,atadensityof1.0×10~4/mL,wasseparatelyharvestedfromsixsamples,whichservedasgroupA.Atotalof1mLAMSCs,atadensityof1.0×10~4/mL,washarvestedseparatelyfromtheremainingsixsamples,whichservedasgroupB.Atotalof0.5mLfromthesixsamplesofgroupAand0.5mLfromthesixsamplesofgroupBwerecombinedtoformgroupC.MAINOUTCOMEMEASURES:Differencesincellquantityamongthethreegroupswerecomparedbycellquantificationand3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide(MTT)analysis.Expressionofaglialcellmarker,neuron-specificenolase,andnestinwasdetectedinthethreegroupsbyimmunocytochemistry.RESULTS:CellquantificationandMTTanalysisoflivecells,aswellasAMSCabsorbance,weresignificantlygreateringroupCcomparedwithgroupsAandBat18daysofculture(P<0.05),andnosignificantdifferencewasobservedbetweengroupsAandB.Glialfibrillaryacidicprotein,neuron-specificenolase,andnestinwereexpressedinallgroupsfollowingbFGFinduction.CONCLUSION:MixedAMSCculturespromotedproliferation,andbFGF-inducedAMSCsdifferentiatedintoneuronal-likecells.

简介：BACKGROUND:Ithasbeendemonstratedthattransforminggrowthfactor-β(TGF-β)andbrain-derivedneurotrophicfactor(BDNF)caninducestemcelldifferentiationintoneuron-likecells.OBJECTIVE:ToinvestigatetheefficacyofTGF-βandBDNFatinducingthedifferentiationofadultratbonemarrowstromalcells(BMSCs)intoneuron-likecells,bothincombinationoralone.DESIGN,TIMEANDSETTING:AcomparativeobservationexperimentwasperformedattheDepartmentofOrthopedics,FirstAffiliatedHospitalofLiaoningMedicalUniversitybetweenOctober2007andJanuary2008.MATERIALS:TGF-βandBDNFwerepurchasedfromSigma,USA;mouseanti-ratneuronspecificenolase,neurofilamentandglialfibrillaryacidicproteinwerepurchasedfromBeijingHMHLBiochemLtd.,China.METHODS:BMSCswereisolatedfromratsaged4weeksandincubatedwithTGF-β(1μg/L)and/orBDNF(50μg/mL).MAINOUTCOMEMEASURES:Expressionofneuron-specificenolase,neurofilamentandglialfibrillaryacidicproteinweredeterminedbyimmunocytochemistry.RESULTS:BMSCsdifferentiatedintoneuron-likecellsfollowinginductionofTGF-βandBDNF,andexpressedbothneuron-specificenolaseandneurofilament.ThepercentofpositivecellswassignificantlygreaterinthecombinationgroupthanthoseinducedwithTGF-βorBDNFalone(P<0.01).CONCLUSION:TreatmentofBMSCswithacombinationofTGF-βandBDNFinduceddifferentiationintoneuron-likecells,withtheinductionbeingsignificantlygreaterthanwithTGF-βorBDNFalone.

简介：

简介：Carbonnanotubescancarryproteinintocellstoinducebiologicaleffects.Amino-functionalizedcarbonnanotubesaresolubleandbiocompatible,havehighreactivityandlowtoxicity,andcanhelppromotenervecellgrowth.Inthisstudy,amino-functionalizedethylenediamine-treatedmulti-walledcarbonnanotubeswereusedtopreparecarbonnanotubes-nervegrowthfactorcomplexesbynon-covalentgrafting.Thephysicochemicalproperties,cytotoxicitytoPC12andchickembryodorsalrootganglion,andbiologicalactivityofthecarbonnanotubes-nervegrowthfactorcomplexeswereinvestigated.Theresultsshowedthataminofunctionalizationimprovedcarbonnanotubes-nervegrowthfactorcomplexdispersibility,reducedtheirtoxicitytoPC12cells,andpromotedPC12celldifferentiationandchickembryodorsalrootganglion.

简介：Thisstudyaimedtoexploretheroleofmechanicaltensioninhypertrophicscarsandthechangeinnervedensityusinghematoxylin-eosinstainingandS100immunohistochemistry,andtoobservetheexpressionofnervegrowthfactorbywesternblotanalysis.Theresultsdemonstratedthatmechanicaltensioncontributedtotheformationofahyperplasticscarinthebackskinofrats,inconjunctionwithincreasesinbothnervedensityandnervegrowthfactorexpressioninthescartissue.Theseexperimentalfindingsindicatethatthecutaneousnervoussystemplaysaroleinhypertrophicscarformationcausedbymechanicaltension.

简介：Ciliaryneurotrophicfactoristheonlyknownneurotrophicfactorthatcanpromotedifferentiationofhippocampalneuralprogenitorcellstoglialcellsandneuronsinadultrats.Thisprocessissimilartospontaneousdifferentiation.Therefore,ciliaryneurotrophicfactormaybeinvolvedinspontaneousdifferentiationofneuralstemcells.Toverifythishypothesis,thepresentstudyisolatedneuralprogenitorcellsfromadultmaleratsandculturedtheminvitro.Resultsshowedthatwhenneuralprogenitorcellswereculturedintheabsenceofmitogenfibroblastgrowthfactor-2orepidermalgrowthfactor,theyunderwentspontaneousdifferentiationintoneuronsandglialcells.Westernblotandimmunocytochemicalstainingshowedthatexogenousciliaryneurotrophicfactorstronglyinducedadulthippocampalprogenitorcellstodifferentiateintoneuronsandglialcells.Moreover,passage4adulthippocampalprogenitorcellsexpressedhighlevelsofendogenousciliaryneurotrophicfactor,andaneutralizingantibodyagainstciliaryneurotrophicfactorpreventedthespontaneousneuronalandglialdifferentiationofadulthippocampalprogenitorcells.Theseresultssuggestthatthespontaneousdifferentiationofadulthippocampalprogenitorcellsismediatedpartiallybyendogenousciliaryneurotrophicfactor.

简介：Gastrodin,anactivecomponentoftallgastrodiatuber,iswidelyusedinthetreatmentofdizziness,paralysis,epilepsy,strokeanddementia,andexhibitsaneuroprotectiveeffect.AratmodelofspinalcordinjurywasestablishedusingAllen’smethod,andgastrodinwasadministeredviathesubarachnoidcavityandbyintraperitonealinjectionfor7days.Resultsshowthatgastrodinpromotedthesecretionofbrain-derivedneurotrophicfactorinratswithspinalcordinjury.Aftergastrodintreatment,themaximumangleoftheinclinedplanetest,andtheBasso,BeattieandBresnahanscoresincreased.Moreover,gastrodinimprovedneuraltissuerecoveryintheinjuredspinalcord.Theseresultsdemonstratethatgastrodinpromotesthesecretionofbrain-derivedneurotrophicfactor,contributestotherecoveryofneurologicalfunction,andprotectsneuralcellsagainstinjury.

简介：BACKGROUND:Pattern-visualevokedpotential(PVEP)canreflectthefunctionalstatusofretinalganglialcells(RGC)andvisualcortex,andisanobjectiveexaminationforvisualpathwayfunction.Itisauniquemethodforobjectivelyexaminingtheopticnervefunctionofopticganglioncells.OBJECTIVE:Toobservetheeffectsofnervegrowthfactor(NGF)onPVEFinthetreatmentofopticnervecontusion,evaluatetheclinicalefficacyofNGF,andmakeanefficacycomparisonwithvitaminB12.DESIGN:Arandomlygrouping,controlledobservation.SETTING:DepartmentofOphthalmology,TangshanGongrenHospitalAffiliatedtoHebeiMedicalUniversity.PARTICIPANTS:Fortypatientswithopticnervecontusioncausedbyeyetrauma,whoreceivedthetreatmentintheTangshanWorkerHospitalAffiliatedtoHebeiMedicalUniversitybetweenJanuary2006andJune2007,wererecruitedinthisstudy.Theinvolved40patients,including34malesand6females,wereaged14-59years.TheywereconfirmedtohaveopticnervecontusionbyophthalmologicconsultationcombinedwithhistoryofdiseaseandorbitalCTexamination.Informedconsentsoftreatmentsanddetecteditemswereobtainedfromallthepatients.Thepatientswererandomlydividedinto2groupswith20ineach:NGFgroupandvitaminB12group.METHODS:Conservativetreatmentwasusedinthetwogroups.Inaddition,patientsintheNGFgroupwereintramuscularlyinjectedwithNGFsolution18μg/time,onceaday.ThoseinthevitaminB12groupwereinjectedbythesamemethodwithcommonvitaminB12of500μgcombinedwithvitaminB1of100mg,onceaday.MAINOUTCOMEMEASURES:PVEPexaminationwasconductedinallthepatientsbefore,oneandtwoweeksaftertreatment,andlatencyandamplitudeatP100weredetected.RESULTS:Fortypatientswithopticnervecontusionparticipatedinthefinalanalysis.Beforetreatment,significantdifferencesinthelatencyandamplitudeatP100werenotfoundinpatientsbetweentwogroups(P>0.05).ForeachpatientintheNGF

简介：BACKGROUND:ThepharmacologicalactionoftraditionalChinesemedicinecompoundisthecomprehensiveeffectofthevariousingredients,andtheinteractionsofvariousingredientsarecloselycorrelatedwiththefinaleffect.InordertorevealthecompatibilitymechanismofBHD'sprescriptionintreatingandpreventingischemiccerebrovasculardisease,weneededexploretheeffectandrelationofingredientsintheprescription.OBJECTIVE:ToobservetheeffectofBuyangHuanwudecoction(BHD)andAstragalusmongholicusontheactivityofplateletactivatingfactorreceptor(PAFR)intheplateletofrabbitsinvitro,andinvestigatethemechanismofAstragalusmongholicus.DESIGN:Adecomposedrecipesstudy.SETTING:GuangzhouUniversityofTraditionalChineseMedicine.MATERIALS:FiveNewZealandrabbits,weighing2-3kg,bothsexes,wereused.BHDwascomposedofShengHuangQi120g,DangGuiWei6g,ChiShao4.5g,ChuanXiong3g,DiLong3g,TaoRen3g,HongHua3g.TheprescriptionforactivatingbloodcirculationconsistedofDangGuiWei6g,ChiShao4.5g,ChuanXiong3g,DiLong3g,TaoRen3gandHongHua3g.Theprescriptionforinvigoratingqiconsistedof120gShengHuangQi.ThepreparedherbalpieceswerepurchasedfromthetraditionalChinesemedicineDispensaryofFoshanSecondPeople'sHospital,andappraisedbyProfessorXufromScienceofChineseMateriaMedicaCollege,GuangzhouUniversityofTraditionalChineseMedicine.3H-PAFwassuppliedbyAmershamCo.,Ltd.(specificactivity:6.475TBq/mmol;batchnumber:200402);PAFstandardbyBiomolCo.,Ltd.(batchnumber:P1318V).METHODS:TheexperimentswerecarriedoutintheLaboratoryofNuclearMedicine,GuangzhouUniversityofTraditionalChineseMedicinefromSeptembertoDecember2004.①InjectionsofBHD,prescriptionsforactivatingbloodcirculationandinvigoratingqiwerepreparedbythedecoctionandalcoholsedimentationtechnique.Rabbitcommoncarotidarteryblood(40mL)wasdrawnviaintubationtoprepareplateletsuspensionof(0.8-1.0)×1010L-1.②Determinationo

简介：Hypoxia-induciblefactor1(HIF-1)attenuatesamyloid-betaproteinneurotoxicityanddecreasesapoptosisinducedbyoxidativestressorhypoxiaincorticalneurons.Inthisstudy,weconstructedarecombinantadeno-associatedvirus(rAAV)vectorexpressingthehumanHIF-1αgene(rAAV-HIF-1α),andtestedtheassumptionthatrAAV-HIF-1αrepresseshippocampalneuronalapoptosisinducedbyamyloid-betaprotein.OurresultsconfirmedthatrAAV-HIF-1αsignificantlyreducesapoptosisinducedbyamyloid-betaproteininprimaryculturedhippocampalneurons.DirectintracerebralrAAV-HIF-1αadministrationalsoinducedrobustandprolongedHIF-1αproductioninrathippocampus.SinglerAAV-HIF-1αadministrationresultedindecreasedapoptosisofhippocampalneuronsinanAlzheimer’sdiseaseratmodelestablishedbyintracerebroventricularinjectionofaggregatedamyloid-betaprotein(25–35).OurinvitroandinvivofindingsdemonstratethatHIF-1haspotentialforattenuatinghippocampalneuronalapoptosisinducedbyamyloid-betaprotein,andprovidesexperimentalsupportfortreatmentofneurodegenerativediseasesusinggenetherapy.

简介：Atpresent,thereisnoeffectivetreatmentfortherepairoftheopticnerveafterinjury,orimprovementofitsmicroenvironmentforregeneration.Intravitreallyinjectedciliaryneurotrophicfactor(CNTF)andolfactoryensheathingcells(OECs)promotethelong-distanceregrowthofseveredopticnervefibersafterintracranialinjury.Here,weexaminedtheefficacyofthesetechniquesaloneandincombination,inaratmodelofopticnerveinjury.WeinjectedcondensedOECsuspensionatthesiteofinjury,orCNTFintothevitreousbody,orbothsimultaneously.Retrogradetracingtechniquesshowedthat4weekspostoperatively,thenumberofsurvivingretinalganglioncellsandtheiraxonaldensityintheopticnerveweregreaterinratssubjectedtoOECinjectiononlythaninthosereceivingCNTFinjectiononly.Furthermore,combinedOEC+CNTFinjectionachievedbetterresultsthaneithermonotherapy.ThesefindingsconfirmthatOECsarebetterthanCNTFatprotectinginjuredneuronsintheeye,butthatcombinedOECandCNTFtherapyisnotablymoreeffectivethaneithertreatmentalone.

简介：Outdoorairpollutionisaknownriskfactorformortalityandmorbidity.Thetypeofairpollutantmostreliablyassociatedwithdiseaseisparticulatematter(PM),especiallyfinerparticulatematterthatcanreachdeeperintothelungslikePM_(2.5)(particulatematterdiameter<2.5μm).SomesubpopulationsmaybeparticularlyvulnerabletoPMpollution.Thisreviewfocusesononesubgroup,long-termstrokesurvivors,andtheemergingevidencesuggestingthatsurvivorsofastrokemaybeatahigherriskfromthedeleteriouseffectsofPMpollution.Whilethemechanismsformortalityarestillunderdebate,long-termstrokesurvivorsmaybevulnerabletosimilarmechanismsthatunderliethewell-establishedassociationbetweenPMpollutionandcardiovasculardisease.Thefactthatlong-termstrokesurvivorsofischemic,butnothemorrhagic,strokesappeartobemorevulnerabletotheriskofdeathfromhigherPMpollutionmayalsobolstertheconnectiontoischemicheartdisease.SurvivorsofanischemicstrokemaybemorevulnerabletodyingfromhigherconcentrationsofPMpollutionthanthegeneralpopulation.TheclinicalimplicationsofthisassociationsuggestthatreducedexposuretoPMpollutionmayresultinfewerdeathsamongststrokesurvivors.

简介：Neuroprotectionbyischemicpreconditioninghasbeenconfirmedbymanystudies,buttheprecisemechanismremainsunclear.Inthepresentstudy,weperformedcerebralischemicpreconditioninginratsbysimulatingatransientischemicattacktwice(eacha20-minuteocclusionofthemiddlecerebralartery)beforeinducingfocalcerebralinfarction(2hourocclusion-reperfusioninthesameartery).Wealsoexploredthemechanismunderlyingtheneuroprotectiveeffectofischemicpreconditioning.Sevendaysafterocclusion-reperfusion,tetrazoliumchloridestainingandimmunohistochemistryrevealedthattheinfarctvolumewassignificantlysmallerinthegroupthatunderwentpreconditioningthaninthemodelgroup.Furthermore,vascularendothelialgrowthfactorimmunoreactivitywasconsiderablygreaterinthehippocampalCA3regionofpreconditionedratsthanmodelrats.Ourresultssuggestthattheprotectiveeffectsofischemicpreconditioningonfocalcerebralinfarctionareassociatedwithupregulationofvascularendothelialgrowthfactor.

简介：BACKGROUND:Brainischemiainvolvessecondaryinflammation,whichsignificantlycontributestotheoutcomeofischemicinsults.Vascularendothelialgrowthfactor(VEGF)mayplayanimportantroleinthevascularresponsetocerebralischemia,becauseischemiastimulatesVEGFexpressioninthebrain,andVEGFpromotesformationofnewcerebralbloodvessels.Minocycline,atetracyclinederivative,protectsagainstcerebralischemiaandreducesinflammation,oxidativestress,andapoptosis.OBJECTIVE:ToobservetheinfluenceofminocyclineonVEGF,interleukin-1beta(IL-1β),andtumornecrosisfactoralpha(TNF-α)expressioninWistarratswithfocalcerebralischemia/reperfusioninjury,andtostudytheneuroprotectionmechanismofminocyclineagainstfocalcerebralischemia/reperfusioninjury.DESIGN,TIMEANDSETTING:Randomized,controlledexperiment,whichwasperformedintheChongqingKeyLaboratoryofNeurologybetweenMarch2007andMarch2008.MATERIALS:Atotalof36female,Wistarratsunderwentsurgerytoinsertathreadintotheleftmiddlecerebralartery.Animalswererandomlydividedintosham-operation,minocyclinetreatment,andischemia/reperfusiongroups,with12ratsineachgroup.Minocycline(HuishiPharmaceuticalLimitedCompany,China)wasdissolvedto0.5g/Linnormalsaline.METHODS:A0.5-1.0cmthreadwasinsertedintoratsfromthesham-operationgroup.Ratsintheischemia/reperfusiongroupunderwentischemiaandreperfusion.Theminocyclinegroupreceivedminocycline(50mg/kg)12and24hoursfollowingischemiaandreperfusion,whereastheothergroupsreceivedsalineatthecorrespondingtimepoints.MAINOUTCOMEMEASURES:mRNAandproteinexpressionofIL-1βandTNF-αwasmeasuredbyreversetranscriptase-polymerasechainreaction(RT-PCR)andenzymelinkedimmunosorbentassay(ELISA),respectively.VEGFmRNAandproteinexpressionwasexaminedbyRT-PCR,Westernblot,andELISA.RESULTS:Minocyclinedecreasedthefocalinfarctvolume.VEGF,IL-1β,andTNF-αexpressionw

简介：Endothelialprogenitorcellsareresidentinthebonemarrowbloodsinusoidsandcirculateintheperipheralcirculation.Theymobilizefromthebonemarrowaftervascularinjuryandhometothesiteofinjurywheretheydifferentiateintoendothelialcells.Activationandmobilizationofendothelialprogenitorcellsfromthebonemarrowisinducedviatheproductionandreleaseofendothelialprogenitorcell-activatingfactorsandincludesspecificgrowthfactorsandcytokinesinresponsetoperipheraltissuehypoxiasuchasafteracuteischemicstrokeortrauma.Endothelialprogenitorcellsmigrateandhometospecificsitesfollowingischemicstrokeviagrowthfactor/cytokinegradients.Somegrowthfactorsarelessstableunderacidicconditionsoftissueischemia,andsyntheticanaloguesthatarestableatlowpHmayprovideamoreeffectivetherapeuticapproachforinducingendothelialprogenitorcellmobilizationandpromotingcerebralneovascularizationfollowingischemicstroke.

简介：BACKGROUND:Ithasbeenshownthatginsenoside,theeffectivecomponentofginseng,canenhanceexpressionofcholineacetyltransferase,aswellasbrain-derivedneurotrophicfactor(BDNF)anditsreceptortyrosinekinaseB(TrkB),incholinergicneuronsofthebasalforebrain.OBJECTIVE:ToqualitativelyandquantitativelyverifytheinfluenceofginsenosideonexpressionofBDNFanditsreceptor,TrkB,inthemedialseptumofagedrats,andtoprovideamolecularbasisforclinicalapplication.DESIGN,TIMEANDSETTING:Acontraststudy,whichwasperformedintheDepartmentofAnatomy,ChinaMedicalUniversity,andtheDepartmentofAnatomy,ShenyangMedicalCollegebetweenDecember2005andMay2007.MATERIALS:Thirty-five,healthy,female,SpragueDawleyratswereselectedforthisstudy.Ginsenoside(81%purity)wasprovidedbyJilinJi’anWantaiChineseMedicineFactory;anti-BDNFantibody,anti-TrkBantibody,andtheirkitswereprovidedbyWuhanBosterCompany.METHODS:Atotalof35ratsweredividedintothreegroups:young(fourmonthsold),aging(26monthsold),andginsenoside.Ratsintheginsenosidegroupwereadministeredginsenoside(25mg/kg/d)between17monthsand26months.MAINOUTCOMEMEASURES:ImmunohistochemistryandinsituhybridizationwereusedtomeasureexpressionofBDNFandTrkBinthemedialseptumofagedrats,andthedetectedresultswereexpressedasgrayvalues.RESULTS:①Qualitativedetection:usingmicroscopy,degenerativeneuronswerevisibleinthemedialseptumintheaginggroup.However,neuronalmorphologyintheginsenosidegroupwassimilartoneuronsintheyounggroup.②Quantitativedetection:themeangrayvalueofBDNF-positiveandTrkB-positiveproductsintheaginggroupweresignificantlyhigherthanintheyounggroup(t=3.346,4.169,P<0.01);however,themeangrayvalueintheginsenosidegroupwassignificantlylowerthanintheaginggroup(t=2.432,2.651,P<0.01).CONCLUSION:GinsenosidecanincreaseexpressionofBDNFandTrkBinth

简介：Angiogenesisintheinfarctperipherycanimprovebloodflow.Vascularendothelialgrowthfactor(VEGF)hasbeenconsideredapotentialtherapeutictargetforstroke.BuyangHuanwudecoction(BYHWD)isaclassictraditionalformulaintraditionalChinesemedicineandisusedtotreatstroke;inaddition,thepromotioneffectsonVEGFproteinexpressionhavebeenconfirmed.However,littleisknownabouthowBYHWDregulatesangiogenesis,orabouttheeffectsofBYHWDonVEGFmRNAexpression.Forthisreason,thepresentstudymeasuredmicrovesseldensityinratswithcerebralischemiausingimmunohistochemistry.Inaddition,VEGFexpressionwasmeasuredbyreverse-transcriptionpolymerasechainreactionandenzyme-linkedimmunosorbentassaytode-terminetheeffectsofBYHWDonangiogenesisandVEGFexpressioninratswithcerebralischemia.Resultsdemonstratedthatmicrovesseldensity,aswellasVEGFmRNAandproteinexpression,increasedafter7and14daysofBYHWDtreatment,whichsuggeststhatBYHWDpromotedan-giogenesisfollowingcerebralischemiaandupregulatedVEGFmRNAandproteinexpressioninischemiccerebralregions.

简介：Parkinson’sdisease(PD)ischaracterizedbytheprogressivelossofmidbraindopaminergic(mDA)neuronsandasubsequentdecreaseinstriataldopaminelevels,whichcausethetypicalclinicalmotorsymptomssuchasmusclerigidity,bradykinesiaandtremor.Althoughasubsetof

简介：Abducensnervepalsy(ANP)iscommonlyseeninpatientswithdiabetesmellitus.ThevalidityofacupunctureasatraditionalChinesemedicinemethodinperipheralnerverepairiswellestablished.However,itsefficacyinrandomizedcontrolledtrialsremainsunclear.Herein,wedesignedaprotocolforaprospective,single-center,randomizedcontrolledtrialtoinvestigatetheeffectofintraorbitalelectroacupunctureondiabeticANP.Weplantorecruit60patientswithdiabeticANP,andrandomlydividethemintotreatmentandcontrolgroups.Patientsinbothgroupswillcontinuetheirglucose-loweringtherapy.Aneuralnutritiondrugwillbegiventobothgroupsforsixweeks.Thetreatmentgroupwillalsoreceiveintraorbitalelectroacupuncturetherapy.Wewillassessefficacyoftreatment,eyeballmovement,diplopiadeviationandthelevelsoffastingblood-glucoseandglycosylatedhemoglobinbeforetreatmentat2,4,and6weeksaftertreatment.Theefficacyandrecurrencewillbeinvestigatedduringfollow-up(1monthafterintervention).ThisprotocolwasregisteredatChineseClinicalTrialRegistryon16January2015(ChiCTR-IPR-15005836).ThisstudywasapprovedbytheEthicsCommitteeofFirstAffiliatedHospitalofHarbinMedicalUniversityofChina(approvalnumber:201452).AllprotocolswillbeinaccordancewithDeclarationofHelsinki,formulatedbytheWorldMedicalAssociation.Writteninformedconsentwillbeprovidedbyparticipants.WeenvisagethattheresultsofthisclinicaltrialwillprovideevidenceforpromotingclinicaluseofthisnewtherapyformanagementofANP.

简介：BACKGROUND:Studieshavedemonstratedthatbrain-derivedneurotrophicfactor(BDNF)hasadualeffectonepilepsy.However,therelationshipbetweenepilepsy-inducedbraininjuryandBDNFremainspoorlyunderstood.OBJECTIVE:Accordingtoultrastructuralandmolecularparameters,todetectthedegreeofneuronalinjuryandBDNFexpressionchangesatdifferentbrainregionsanddifferentkindlingtimestodeterminetheeffectsofBDNFonepilepsy-inducedbraininjury.DESIGN,TIMEANDSETTING:Arandomized,controlled,animalexperimentbasedonneuropathologyandmolecularbiologywasperformedattheDepartmentofPhysiologyandDepartmentofPathology,BasicMedicalCollegeofJilinUniversityin2003.MATERIALS:UltraSensitiveSPkitforimmunohistochemistry(FuzhouMaximBiotechnology,China),BDNFantibody(concentratedtype,WuhanBosterBiologicalTechnology,China),JEM-1000SXtransmissionelectronmicroscopy(JEOL,Japan),andBH-2lightmicroscope(Olympus,Japan)wereusedinthepresentstudy.METHODS:Wistarratswererandomlyassignedtocontrol(n=6),sham-surgery(n=6),andmodel(n=60)groups.Thecontrolgroupratswerenottreated;anelectrodewasembeddedintotheamygdalainratsfromthesham-surgeryandmodelgroups;anamygdalakindlingepilepsymodelwasestablishedinthemodelgroup.MAINOUTCOMEMEASURES:Pathologicalchangesinthetemporallobeandhippocampuswereobservedbylightandelectronmicroscopyat1,3,7,14,and21daysfollowingkindling,andBDNFexpressioninthevariousbrainregionswasdeterminedbyimmunohistochemistry.RESULTS:Inthemodelgroup,temporallobecorticalandhippocampalneuronswereswollenandthenucleiwerelaterallydeviated.Therewerealsosomeapoptoticneurons3daysafterkindling.Thenucleolidisappearedandthenucleiappearedbrokenorlysed,aswellasslightmicrogliahyperplasia,at7days.Electronmicroscopicobservationdisplayedchromatinaggregationinthenucleiandslightmitochondrionswelling3daysafterkindling.Injurychangeswereaggravatedat7days,characteriz