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简介：Hypemecrospenniaisthecommondiseasefrequentlyseeninandriatry.It'soneofthemainreasonsthatcausethemasculinesterility.DuringMarch1997December2003.Theauthorapplieddecoctionfortonifyingthekidneyandgeneratingthespermintreatmentofthisdiseaseandreceivedrathergoodefficacy.Thecompletesummaryof136caseswasreportedasfollowed.

简介：ShouwuisatraditionalChinesemedicine(TCM)withneuroprotectiveeffect.ShouwuYizhidecoction(SYD)wasdesignedbasedonTCMtheory.However,littleisknownabouttherolesofSYDinVasculardementia(VaD).ThepresentstudyaimedtoevaluatethepotentialeffectsofSYDonthevascularcognitiveimpairmentandexploretheunderlyingmechanismbyestablishingfocalcerebralischemia/reperfusion(I/R)ratmodeltoinduceVaD.SYDadministration(54mg·kg~(-1))for40daysobviouslyimprovedthevascularcognitiveimpairmentinthemiddlecerebralarteryocclusion(MCAO)ratsasevidencedbythedeclinedneurologicaldeficitscoreandshortenedescapelatencyvianeurologicaldeficitassessmentandMorriswatermazetest.Moreover,SYDdecreasedneurondamage-inducedcelldeathandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,therebyalleviatingVaD.Mechanistically,SYDcausedincreasesintheexpressionofvascularendothelialgrowthfactor(VEGF),CD34andCD31,comparedwiththeMCAOratsincoronalhippocampus.Simultaneously,theexpressionlevelofmiR-210waselevatedsignificantlyafterSYDadministration,comparedwiththevehiclerats(P<0.01).TheexpressionofNotch4atbothmRNAandproteinlevelswasupregulatedremarkablyalongwiththenotablydownregulatedDLL4expressionunderSYDadministrationcomparedwiththevehiclerats(P<0.05).Overall,theaboveresultsindicatedthatSYDpromotedangiogenesisbyupregulatingVEGF-inducedmiR210expressiontoactivateNotchpathway,andfurtheralleviatedneurondamageandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,ultimatelyenhancingthecognitionandmemoryofMCAOrats.Therefore,ourfindingspreliminarilyidentifiedtheeffectandthemechanismofactionforSYDonVaDinrats.SYDcouldbeapotentialcandidateintreatmentofVaD.

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

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简介：ToinvestigatetheprotectiveeffectofdecoctionofliaoweiongastricmucosaofH.pyloriassociatedchronicatrophicgastritisinrats.TheH.pyloriassociatedchronicatrophicgastritismodelswereinducedwithsodiumdeoxycholate,sodiumsalicylate,ethanol,andculturebrothofH.pylori.ProtectiveeffectofdecoctionofliaoweiongastricmucosaofH.pyloriassociatedchronicatrophicgastritiswasobservedquantitatively.

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：BACKGROUND:Argininevasopressinhasbeenshowntoenhancelearninginexperimentalanimalmodels.OBJECTIVE:TodeterminewhetherGuipidecoctionenhancesmemoryandlearningbyincreasingargininevasopressinlevels,andtoverifytheinfluenceofGuipidecoctiononargininevasopressinproteinandgeneexpressioninthehippocampalCA1region,prefrontallobecortex,andventralnucleusofhypothalamusinratswithspleendeficiency.DESIGN,TIMEANDSETTING:Therandomized,neuropharmacological,controlstudywasperformedintheCollegeofBasicMedicalSciences,BeijingUniversityofChineseMedicinebetweenMarch2002andMarch2005.MATERIALS:Sixty,healthy,male,WistarratswereusedtoestablishspleendeficiencymodelsaccordingtothetraditionalChinesemedicineprincipleofbitterdrugsforpurgation,improperdiet,andoverstrain.Argininevasopressin-1polyclonalanti-rabbitantibodyimmunohistochemistrykitandargininevasopressininsituhybridizationkitwereprovidedbyDepartmentofNeuroanatomyinShanghaiSecondMilitaryMedicalUniversityofChinesePLA.METHODS:Sixtyratsweredividedintofivegroupsatrandom:normalcontrol(n=11),model(n=13),Guipidecoction(n=12),recipecontrolA(n=12),andrecipecontrolBgroups(n=12).Ratsinthelatterfourgroupsreceived7.5g/kgofthedrugsbyintragastricadministrationeachmorning,whichcomprisedDahuang,Houpu,andZhishi,preparedataratioof2:1:1.Theratswerefastedeveryotherday,butwereallowedfreeaccesstowateratalltimes.Theratswereforcedtoswimin25℃wateruntilfatigued.RatsintheGuipidecoctionandtworecipecontrolgroupswereintragastricallyadministered7.5g/kgGuipidecoction,ChaihuShuganpowder,andTianwangBuxinpellets,respectively,eachafternoon.Ratsinthenormalgroupwereintragastricallyadministeredthesameamountofnormalsaline.Allratsweretreatedfor6weeks.MAINOUTCOMEMEASURES:At6weeksafterdrugadministration,ratbraintissueswereharvested.Ar

简介：Theuterinetetaniccontractionanduterinearterybloodflowreductionarepossiblereasonsforprimarydysmenorrhea（PD）.Inthepresentstudy,weaimedtoevaluatetheuterinerelaxanteffectandtheinfluenceonuterinearterybloodvelocityofGe-GenDecoction（GGD）,awell-knownChineseherbalformula.InfemaleICRmice,uterinecontractionwasinducedbyoxytocinexposurefollowingestradiolbenzoatepretreatment,andtheuterinearterybloodvelocitywasdetectedbyDopplerultrasound.HistopathologicalexaminationoftheuterinetissuesampleswereperformedbyH&Estaining.Exvivostudiesdemonstratedthatoxytocin,posteriorpituitary,oracetylcholineinducedcontractionsinisolatedmouseuterus.GGDinhibitedbothspontaneousandstimulatedcontractions.InvivostudydemonstratedthatGGDsignificantlyreducedoxytocin-inducedwrithingresponseswithamaximalinhibitionof87%.FurtherstudydemonstratedthatGGDnormalizedoxytocin-inducedabnormalitiesofprostaglandinsF2alpha(PGF2α)andCa2+inmice.Inaddition,injectionofoxytocininducedadecreaseinuterinearterybloodflowvelocity.PretreatmentwithGGDreversedtheoxytocinresponseonbloodflowvelocity.HistopathologicalexaminationshowedpretreatmentwithGGDalleviatedinflammationandedemaintheuteruswhencomparedwiththemodelgroup.BothexvivoandinvivoresultsindicatedthatGGDpossessedasignificantspasmolyticeffectonuterinetetaniccontractionaswellasimprovementonuterinearterybloodvelocitywhichmayinvolvePGF2αandCa2+signaling,suggestingthatGGDmayhaveaclinicpotentialinPDtherapy.

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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：AIMToexploretheprotectiveeffectsandunderlyingmechanismsoftotalpolysaccharidesoftheSijunzidecoction(TPSJ)ontheepithelialbarriersinvitro.METHODSCaco-2cellmonolayersweretreatedwithorwithoutTPSJinthepresenceorabsenceofTNF-α,andparacellularpermeabilityandtransepithelialelectricalresistance(TEER)weremeasuredtoevaluatetheepithelialbarrierfunction.Immunofluorescenceandwesternblottingwererespectivelyusedtoevaluatethedistributionandexpressionofthetightjunctionproteinsclaudin1,claudin2,zo3,andoccludininCaco-2cells.Westernblottingwasalsousedtoevaluatethecellularexpressionofmyosinlightchain(MLC),phosphorylatedMLC(pMLC),MLCkinase(MLCK),andnuclearfactor(NF)-κBp65.RESULTSTPSJpromotedtheproliferationofCaco-2cellsandinhibitedTNF-α-inducedsecretionofpro-inflammatorycytokines.Furthermore,TPSJsignificantlyamelioratedboththereductionofTEERandtheincreasedparacellularpermeabilityobservedintumornecrosisfactor(TNF)-α-damagedCaco-2monolayers.Furthermore,TPSJremarkablyattenuatedTNF-α-inducedmorphologicalchanges,downregulatedtheexpressionofclaudin1,claudin2,zo3,andoccludin,andmarkedlysuppressedTNF-α-mediatedupregulationofp-MLCandMLCKexpression.Finally,TPSJinhibitedtheactivationandexpressionofNF-κBp65.CONCLUSIONOurresultsdemonstratethatTPSJalleviatestheTNF-α-inducedimpairmentoftheintestinalepithelialcellbarrierfunctionbysuppressingNF-κBp65-mediatedphosphorylationofMLCKandMLC.