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: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：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.

简介：1-methyl-4-phenylpyridiniumion(MPP+)inducesendoplasmicreticulumstressandactivatescaspase-12inPC12cells,leadingtoneuronalapoptosis.However,theunderlyingmolecularmechanismremainsunknown.Thepresentstudyinvestigatedtheregulatoryeffectsofnervegrowthfactor(Aktactivator)andlithiumchloride(glycogensynthasekinase-3βinhibitor)ontheendoplasmicreticulumstresssignalingpathway.TheresultsrevealedthatMPP+inducedexpressionofBipandC/EBPhomologousprotein.TheupregulationofBipandC/EBPhomologousprotein,aswellasthedecreasedpro-caspase-12levelinducedbyMPP+wereinhibitedbypretreatmentofthenervegrowthfactororlithiumchloride.Theseresultssuggestthatthephosphatidylinositol3kinase-Akt-glycogensynthasekinase-3βpathwayisinvolvedinMPP+-inducedendoplasmicreticulumstress.