简介：BACKGROUND:TheprogressivedegenerationofdopaminergicneuronsinParkinson’sdiseaseisassociatedwithanactivatedglialreaction,combinedwithaninflammatoryprocess.Theseresponsesleadtotheproductionofcytokines,suchasinterferon-γ,tumornecrosisfactor-α(TNF-α),andinterleukin-1β.Inaddition,14-3-3proteinisacomponentofLewybodiesinParkinson’sdisease.OBJECTIVE:Toobservetheexpressionof14-3-3γandζprotein,aswellasTNF-α,inmousemicroglia,aswellaschangesafterlipopolysaccharide(LPS)activation.Toinvestigatepossiblemechanismsofdopaminergicneuronalinjuryduetoactivatedmicroglia.ToandclarifytheimmuneresponsemechanismsofParkinson’sdisease.DESIGN:Randomizedcontrolledobservation,cellstudy.SETTING:LaboratoryofDepartmentofNeurology,theAffiliatedUnionHospitalofTongjiMedicalCollege,HuazhongUniversityofScienceandTechnology.MATERIALS:TheBV-2immortalizedmurinemicrogliacelllinewaspurchasedfromChinaUnitcellcenter.LPSwasprovidedbySigmaCompany.CellcultureswerepurchasedfromGibco.Phospho-(Ser)14-3-3bindingmotifantibodywaspurchasedfromSantaCruzBiotechnologies.FITCwasprovidedbyLinfeiBiotechnology,Wuhan,China.TNF-αELISAwasprovidedbyJingmeiBiotechCo,Wuhan,China.TheflowcytometerwasprovidedbyBectonDickinson,Canada.METHODS:ThepresentexperimentwasperformedattheLaboratoryofDepartmentofNeurology,theAffiliatedUnionHospitalofTongjiMedicalCollege,HuazhongUniversityofScienceandTechnologyfromApriltoDecember2006.Themicroglialcellline,BV-2,wasculturedinvitroandstimulatedwithLPSfor2,6,12,and24hours.BV-2cultureswithoutLPSwereusedascontrols.MAINOUTCOMEMEASURES:Expressionof14-3-3γproteinwasdetectedbyflowcytometry.14-3-3ζpercentageexpressionandthemeanfluorescenceintensitywasdetectedbyimmunofluorescence.TNF-αexpressionwasdetectedbyELISA.RESULTS:14-3-3γproteinexpressionanalysis:followi

简介：BACKGROUND:ButhusmartensiiKarschisararemedicinalanimal,anddriedintegralButhusmartensiiKarschisanimportantdrugintraditionalChinesemedicine.OBJECTIVE:Toinvestigatetheeffectsofscorpionvenomanalgesicactivepeptide(SAP)extractedfromButhusmartensiiKarschonevokedunitdischargeofthecommonperonealnerveintheposteriornucleusgroupofthethalamususingastereotaxicelectrophysiologicalextracellularmicroelectroderecording.DESIGN,TIMEANDSETTING:One-waydesignedstudy,performedinthePhysiologicalLaboratoryofShenyangMedicalCollegeonSeptember15,2006.MATERIALS:Fifty3-4monthsoldWistarrats(25malesand25females)wereused.SAPwasprovidedbyShenyangPharmaceuticalUniversity.MorphinesolutionwasmadebytheFirstDrugManufactory,NortheasternDrugManufactureGroup(batchnumber:H20013351).NaloxonesolutionwasmadebyHunanPharmaceuticalCo.,Ltd.(batchnumber:H43021669).TypeATAC-350medicaldataprocessingequipmentwasmadebythePhotoelectricityCompany,Japan.METHODS:FiftyratswererandomlydividedintotheSAPgroup(n=20),salinegroup(n=10),morphinegroup(n=10),ornaloxonegroup(n=10).IntheSAPgroup,thecommonperonealnervewasseparatedandstimulatedwithasinglesquarewave(17-19Vintensity;0.2mswidth;20msretardationtime).Subsequently,SAP(0.01%,2μL)wasinjectedintotheposteriornucleusgroupofthethalamus.Ratsinthenaloxonegroupwereinjectedwithnaloxone(1.0mg/kgi.v.)beforeSAPinjection.Ratsinthesalinegroupandthemorphinegroupwereinjectedwithsaline(2μL)ormorphine(0.01%,2μL),respectively,beforeSAPinjection.OtherprocedureswerethesameasthoseintheSAPgroup.MAINOUTCOMEMEASURES:EvokeddischargeintheposteriornucleusgroupofthethalamusandeffectsofSAPaloneandSAPincombinationwithsaline,morphine,ornaloxoneondischargesintheposteriornucleusgroupofthethalamusasmeasuredbyTQ-19medicaldataprocessingequipment.RESULTS:SAPgr

简介：OurpreliminarystudiesconfirmedthatanactiveprincipleregionofBuyangHuanwudecoction,comprisingalkaloid,polysaccharide,aglycon,glucosideandvolatileoil,caninducebonemarrowmesenchymalstemcelldifferentiationintoneurons.Mitogen-activatedproteinkinasesignalingwasidentifiedasoneofthekeypathwaysunderlyingthisdifferentiationprocess.Thepresentstudyshowsphosphorylatedextracellularsignal-regulatedproteinkinaseandphosphorylatedp38proteinexpressionwasincreasedafterdifferentiation.Cellularsignalingpathwayblockingagents,PD98059andSB203580,inhibitedextracellularsignal-regulatedproteinkinaseandp38inmitogen-activatedproteinkinasesignalingpathwaysrespectively.mRNAandproteinexpressionoftheneuronalmarker,neuronspecificenolase,andneuralstemcellmarker,nestin,weredecreasedinbonemarrowmesenchymalstemcellsaftertreatmentwiththeactiveprincipleregionofBuyangHuanwudecoction.Experimentalfindingsindicatethat,extracellularsignal-regulatedproteinkinaseandp38inmitogen-activatedproteinkinasesignalingpathwaysparticipateinbonemarrowmesenchymalstemcelldifferentiationintoneuron-likecells,inducedbytheactiveprincipleregionofBuyangHuanwudecoction.