简介：CheonggukjangisasoybeanpastemadebyfermentingwholecookedsoybeanswithBacillussubtilis.Cheonggukjangcontainsafibrinolyticenzymethatcouldprovideclinicalapplicationsforremovingbloodclots.Inthepresentstudy,theterm'cheonggukjangkinase'(CGK)wasusedtorefertothisfibrinolyticenzyme.ThethrombolyticeffectsofCGKwereanalyzedinaratmodelofcerebralembolicstrokeproducedbymiddlecerebralarteryocclusion(MCAO).Resultsfromfibrinandplatelet-richclotlysisassaysdemonstratedthatthrombolyticactivitywasgreatestinCGKs,whichwereculturedfor40hours.Inaddition,T50,thetimeneededtodecompose50%oftheclot,didnotchangewithplasminogentreatment,indicatingthatCGKwasnotaplasminogenactivator,butwasratherpresumedtoactasaplasmin-likeprotein.AnintravenousinfusionofCGK(1Uplasmin-likeactivity/100μgCGK/kg)at1hourafterMCAOresultedinremovalofclotsinaratmodelofcerebralembolicstroke.CGK-treatedgroupsexhibitedasignificantdose-dependentreductionininfarctvolume.CGKtreatmentalsoimprovedfunctionalrecovery,asassessedbyneurologicaldeficitscores.DecreasedinfarctvolumeandimprovedfunctionalrecoveryfollowingCGKtreatmentwasgreatercomparedwithrecombinanttissueplasminogenactivator(10mg/kg).TheseresultssuggestedthatCGKeffectivelyreducedinfarctvolumeandimprovedfunctionalrecoveryfollowingischemicbraininjury.CGKexhibitsanumberofpotentialclinicalapplicationsinthetreatmentofcerebralembolicstroke.

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：BACKGROUND:RecentstudieshavesuggestedthatmitochondrialATP-sensitiveK+channelopenerscouldreducemyocardiuminfarctsize,andprotectthefunctionofthemitochondria.OBJECTIVE:ToinvestigatethechangesofcerebralinfarctionvolumeandtheactivityofmarkerenzymesinbrainmitochondriaofratsgiventheATP-sensitiveK+channelopener,nicorandil,beforefocalcerebralischemia/reperfusion(I/R).DESIGN,TIMEANDSETTING:Randomized,controlledanimalexperiment,completedattheBrainScientificResearchCenteroftheAffiliatedHospitalofQingdaoUniversityfromJulytoNovember2007.MATERIALS:SixtyhealthymaleWistarratsweighing280–300g.Nicorandil,5-hydroxydecanoate(5-HD)andcytochromeCwerepurchasedfromSigmaintheUSA.Standardmalondialdehyde(MDA)andproteinwerepurchasedfromNanjingJianchengBiotechnologyInstitute.METHODS:Sixtyratswererandomlydividedintoashamoperationgroup,amiddlecerebralarteryocclusion(MCAO)group,anicorandilgroupandanicorandil+5-HDgroup.MCAOfor2hourswasperformedintheMCAOgroup,nicorandilgroupandnicorandil+5-HDgroup.Atotalof5mLsalineweregiventotheMCAOgroupbeforeMCAO.ThenicorandilgroupwasinjectedwiththeATP-sensitiveK+channelopenernicorandil10mg/kgintraperitoneally30minutesbeforeMCAO.Thenicorandil+5-HDgroupwasinjectedwith5-HD10mg/kgintravenously15minutesbeforethesametreatmentasthenicorandilgroup.MAINOUTCOMEMEASURES:Infarctvolumebytotalbrainslicecalculation,activitiesofsuccinatedehydrogenase(SDH)andcytochromeoxidase(CO),andcontentofMDAwereobservedat22hoursofreperfusionafter2hoursMCAO.RESULTS:Sixtyratswereincludedinthefinalanalysis,withoutanyloss.(1)Infarctvolume:comparedwiththeMCAOgroupandnicorandil+5-HDgroup,thepercentageofinfarctvolumewassignificantlydecreasedinthenicorandilgroup(P<0.01).(2)ThecontentofMDA,expressionofSDHandCOinbrain:theexpressionsofSDHandCOintheshamop

简介：BACKGROUND:Animalexperimentshaveconfirmedthatbonemarrowstromalcell(BMSC)transplantationcanserveasatreatmentforepilepsy.OBJECTIVE:BMSCsderivedfromgreenfluorescentprotein(GFP)miceweretransplantedintothehippocampalCA1regionofepilepticrats.Theaimofthestudywastorecordelectroencephalogram(EEG),analyzesurvivalandmigrationofBMSCs,andvalidatetheeffectofBMSCtransplantationforthetreatmentofepilepsy.DESIGN,TIMEANDSETTING:ArandomizedblockdesignexperimentwasperformedattheInstituteofNeuroscience,KunmingMedicalCollegefromMarch2005toFebruary2006.MATERIALS:HomozygousC57BL/6CrSlcTgN(acr-EGFP)OsbC14-Y01-FM131mice,8-12weeksofage,wereselectedforpreparationofcellsuspension.SpragueDawleyratswereselectedforestablishingepilepsymodels.METHODS:Ratswererandomlydividedinto4groups:control(n=8),model(n=8),normalsaline(n=24),andBMSC(n=24).Inthemodel,normalsaline,andBMSCgroups,epilepsywasestablishedwithpenicillin(3×107U/kgi.p.×7days).RatsintheBMSCgroupreceivedaBMSCsuspensionderivedfromgreenfluorescentproteinmiceintotherighthippocampalCA1region.RatsinthevehiclecontrolgroupwereinjectedwiththesamevolumeofnormalsalineintothehippocampalCA1region.MAINOUTCOMEMEASURES:Theelectroencephalogramwasusedtomonitorbrainactivity.SurvivalandmigrationofthetransplantedBMSCswasobservedusingfluorescencemicroscopyat1,2,and4weeksaftertransplantation.RESULTS:InBMSCgroup,fluorescentcellswereobservedatthetransplantationsiteandintheadjacenttissue,aswellasinthetissuesurroundingtheneedletract,indicatingthemigrationofimplantedcells.Fluorescentcellswerenotdetectedinthevehiclecontrolgroup.Theelectroencephalogramofthecontrolanimalsexhibited7-9Hzαwaves,withawaveamplitude<50μV.Inthemodelandvehiclecontrolgroups,randomspike-and-wavedischargesofthesharpspike-sharplowwavetyp

简介：Traumaticinjuriestospinalcordelicitdiversesignalingpathwaysleadingtounselectiveandcomplexpathologicaloutcomes:deathofmultipleclassesofneuralcells,formationofcysticcavitiesandglialscars,disruptionofaxonalconnections,anddemyelinationofsparedaxons,allofwhichcancontributemoreorlesstodebilitatingfunctionalimpairmentsfoundinpatientswithspinal

简介：BACKGROUND:Mailuoning,aChineseherb,hasbeenwidelyusedinChinatotreatacuteischemicstroke,andthemajorcomponentexhibitsanti-oxidativeeffects.However,thepreciseanti-oxidationpathwayremainsuncertain.OBJECTIVE:TovalidatetheprotectiveeffectsofMailuoningonH2O2-inducedprimarycorticalneuroninjuryinembryonicmice.DESIGN,TIMEANDSETTING:ComparativeobservationandinvitroexperimentswereperformedattheJiangsuKeyLaboratoryforMolecularMedicinefromJanuary2008toSeptember2009.MATERIALS:Mailuoning(NanjingJinlingMedicalCompany,China),reactiveoxygenspecies(ROS)kit(BeyotimeBiotechnology,China),superoxidedismutase(SOD),Cu/ZnSODkit,malondialdehyde(MDA)kits(NanjingJiancheng,China),mitochondrialmembranepotential(GMS10013.1,GENMED,USA)andcatalaseactivityassaykit(BeyotimeBiotechnology,China)wereutilizedforthepresentstudy.METHODS:MouseembryoniccorticalneuronswereisolatedandculturedwithculturemediumcontainingH2O2(80μmol/L)and/orMailuoning(1.25μg/mL)for24hours.MAINOUTCOMEMEASURES:Neuronalviabilityanddeathweredetectedbymethylthiazolyltetrazdiumandflowcytometry;ROSproductionwasdeterminedbyflowcytometry;mitochondrialmembranepotentialwasdetectedusingfluorescentstaining;SODactivitywasdetectedusingamodifiednitrobluetetrazoliummethod;Cu/ZnSODandcatalaseactivitywasdetectedbyspectrophotometry;andMDAwasdeterminedusingthelipidperoxidationmethod.RESULTS:H2O2increasedROSproductionandMDAconcentration(P<0.05),anddecreasedmitochondrialmembranepotential,SOD,Cu/ZnSODandcatalaseactivity(P<0.05);thenumberofsurvivingneurons(P<0.05)wasalsoreduced.Mailuoningreversedthesechanges.CONCLUSION:MailuoningprotectsH2O2-inducedinjuryincorticalcellsbyinhibitingROSandMDA,increasingdepolarizationofmitochondrialmembrane,andenhancingSODandcatalaseactivity.

简介：Thestudyaimstoconfirmtheneuroregenerativeeffectsofbacterialmelanin(BM)oncentralnervoussysteminjuryusingaspecialstainingmethodbasedonthedetectionofCa~(2+)-dependentacidphosphataseactivity.Twenty-fourratswererandomlyassignedtoundergoeitherunilateraldestructionofsensorimotorcortex(groupI;n=12)orunilateralrubrospinaltracttransectionatthecervicallevel(C3–4)(groupⅡ;n=12).Ineachgroup,sixratswererandomlyselectedaftersurgerytoundergointramuscularinjectionofBMsolution(BMsubgroup)andtheremainingsixratswereintramuscularlyinjectedwithsaline(salinesubgroup).NeurologicaltestingconfirmedthatBMacceleratedtherecoveryofmotorfunctioninratsfrombothBMandsalinesubgroups.Twomonthsaftersurgery,Ca~(2+)-dependentacidphosphataseactivitydetectionincombinationwithChilingarian'scalciumadenosidetriphosphatemethodrevealedthatBMstimulatedthesproutingoffibersanddilatedthecapillariesinthebrainandspinalcord.TheseresultssuggestthatBMcanpromotetherecoveryofmotorfunctionofratswithcentralnervoussysteminjury;anddetectionofCa~(2+)-dependentacidphosphataseactivityisafastandeasymethodusedtostudytheregeneration-promotingeffectsofBMontheinjuredcentralnervoussystem.