简介：ThepresentstudywasdesignedtodeterminetheeffectsofatraditionalChinesemedicine,calledQishenYiqiDroppingPillonchronichypoxia-inducedmyocardialinjury.ToestablisharatchronichypoxiamodeltobeusedintheevaluationofthetherapeuticeffectsoftheQishenYiqiDroppingPill,Sprague-Dawley(SD)ratswererandomlydividedintothreegroups:thecontrol,model,andtreatmentgroups(n=10pergroup).Theanimalswerehousedinaplexiglasscontainer.Thecontrolanimalswereundernormaloxygenconcentrationandthemodelandtreatmentgroupswereexposedtoairandnitrogenfor5weeks.TheratsinthetreatmentgroupwereorallyadministeredtheQishenYiqiDroppingpill(35mg·kg-1·d-1)for5weeks.Afterthetreatment,thecardiacfunctionandmorphologywereanalyzed,andtheexpressionlevelsofhypoxia-induciblefactor1α(HIF-1α)weredeterminedusingWesternblotting.Ourresultsindicatedthatthecardiacfunctionwasimpaired,cellapoptosiswasenhanced,andHIF-1αexpressionwasup-regulatedinthemodelgroup,comparedtothecontrolgroup.ThesechangeswereamelioratedbythetreatmentwiththeQishenYiqiDroppingPill.Inconclusion,QishenYiqiDroppingpillcanamelioratemyocardialinjuryinducedbychronichypoxia,improvecardiacfunction,anddecreasemyocardialcellapoptosis,whichmayprovideabasisforitsclinicaluseforthetreatmentofchroniccardiovasculardiseases

简介：ThepresentstudywasdesignedtoevaluatetheprotectiveeffectsofethanolextractsofRabdosiajaponicavar.glaucocalyx(Maxim.)Hara(RJ)onlipopolysaccharide(LPS)-inducedacutelunginjury(ALI)inmiceandthepossibleunderlyingmechanismsofaction.ThemicewereorallyadministratedwithRJextract(16,32or64mg?kg–1)dailyforconsecutive7daysbeforeLPSchallenge.Theungspecimensandthebronchoalveolarlavagefluid(BALF)werecollectedforhistopathologicalexaminationsandbiochemicalanalyses.PretreatmentwithRJsignificantlyenhancedsuperoxidedismutase(SOD)activityandreducedthewet-to-dryweight(W/D)ratio,thelevelsofnitricoxide(NO)andproteinleakage,andmyeloperoxidase(MPO)activityinmicewithALI,inadose-dependentmanner.RJreducedcomplementdepositionandsignificantlyattenuatedLPS-inducedALIbyreducingproductionsofinflammatorymediators,suchastumornecrosisfactor-α(TNF-α),interleukin-6(IL-6),andinterleukin-1β(IL-1β).TheresultsdemonstratedthatRJmayattenuateLPS-inducedALIviareducingtheproductionofpro-inflammatorymediators,andreducingcomplementdepositionandradicals.

简介：PhyllanthusUrinariaL.(PUL)isatraditionalChinesemedicineusedtotreathepaticandrenaldisorders.However,themechanismofitshepatoprotectiveactionisnotfullyunderstood.Inthepresentstudy,bloodbiochemicalindexesandliverhistopathologicalchangeswereusedtoestimatetheextentofhepaticinjury.GC/MSandLC/MS-baseduntargetedmetabolomicswereusedincombinationtocharacterizethepotentialbiomarkersassociatedwiththeprotectiveactivityofPULagainstCCl_4-inducedliverinjuryinrats.PULtreatmentcouldreversetheincreaseinALT,ASTandALPinducedbyCCl_4andattenuatethepathologicalchangesinratliver.SignificantchangesinlivermetabolicprofilingwereobservedinPUL-treatedgroupcomparedwithliverinjurymodelgroup.SeventeenbiomarkersrelatedtothehepatoprotectiveeffectsofPULagainstCCl_4-inducedliverinjurywerescreenedoutusingnonparametrictestandPearson'scorrelationanalysis(OPLS-DA).TheresultssuggestedthatthepotentialhepatoprotectiveeffectsofPULinattenuatingCCl_4-inducedhepatotoxicitycouldbepartiallyattributedtoregulatingL-carnitine,taurocholicacid,andaminoacidsmetabolism,whichmaybecomepromisingtargetsfortreatmentoflivertoxicity.Inconclusion,thisstudyprovidesnewinsightsintothemechanismofthehepatoprotectionofPhyllanthusUrinaria.

简介：Ginkgolicacids(GAs),primarilyfoundintheleaves,nuts,andtestaofginkgobiloba,havebeenidentifiedwithsuspectedallergenic,genotoxicandcytotoxicproperties.However,littleinformationisavailableaboutGAstoxicityinkidneysandtheunderlyingmechanismhasnotbeenthoroughlyelucidatedsofar.InsteadofGAsextract,therenalcytotoxicityofGA(15:1),whichwasisolatedfromthetestaofGinkgobiloba,wasassessedinvitrobyusingMDCKcells.TheactionofGA(15:1)oncellviabilitywasevaluatedbytheMTTandneutralreduptakeassays.Comparedwiththecontrol,thecytotoxicityofGA(15:1)onMDCKcellsdisplayedatime-anddose-dependentmanner,suggestingthecellsmitochondriaandlysosomesweredamaged.ItwasconfirmedthatGA(15:1)resultedinthelossofcellsmitochondrialtrans-membranepotential(ΔΨm).Inpropidiumiodide(PI)staininganalysis,GA(15:1)inducedcellcyclearrestattheG0/G1andG2/Mphases,influencingontheDNAsynthesisandcellmitosis.CharacteristicsofnecroticcelldeathwereobservedinMDCKcellsattheexperimentalconditions,asaresultofDNAagarosegelelectrophoresisandmorphologicalobservationofMDCKcells.Inconclusion,thesefindingsmightprovideusefulinformationforabetterunderstandingoftheGA(15:1)inducedrenaltoxicity.

简介：Houttuyniacordatapolysaccharide(HCP)isextractedfromHouttuyniacordata,akeytraditionalChinesemedicine.ThestudywastoinvestigatetheeffectsofHCPonintestinalbarrierandmicrobiotainH1N1virusinfectedmice.MicewereinfectedwithH1N1virusandorallyadministratedHCPatadosageof40mg(kg^-1(d^-1.H1N1infectioncausedpulmonaryandintestinalinjuryandgutmicrobiotaimbalance.HCPsignificantlysuppressedtheexpressionofhypoxiainduciblefactor-1αanddecreasedmucosubstancesingobletcells,butrestoredthelevelofzonulaoccludens-1inintestine.HCPalsoreversedthecompositionchangeofintestinalmicrobiotacausedbyH1N1infection,withsignificantlyreducedrelativeabundancesofVibrioandBacillus,thepathogenicbacterialgenera.Furthermore,HCPrebalancedthegutmicrobiotaandrestoredtheintestinalhomeostasistosomedegree.TheinhibitionofinflammationwasassociatedwiththereducedlevelofToll-likereceptorsandinterleukin-1βinintestine,aswellastheincreasedproductionofinterleukin-10.OraladministrationofHCPalleviatedlunginjuryandintestinaldysfunctioncausedbyH1N1infection.HCPmaygainsystemictreatmentbylocalactingonintestineandmicrobiota.Thisstudyprovedthehigh-valueapplicationofHCP.

简介：ThepresentstudywasdesignedtodeterminetheeffectsofGuanfubaseA(GFA)onthelatesodiumcurrent(INa.L),transientsodiumcurrent(INa.T),HERGcurrent(IHERG),andKv1.5current(IKv1.5).ThevaluesofINa.L,INa.T,IHERGandIKv1.5wererecordedusingthewhole-cellpatchclamptechnique.Comparedwithotherchannels,GFAshowedselectiveblockingactivityinlatesodiumchannel.ItinhibitedINa.Linaconcentration-dependentmannerwithanIC50of(1.57±0.14)μmol·L-1,whichwassignificantlylowerthanitsIC50valuesof(21.17±4.51)μmol·L-1fortheINa.T.TheinhibitoryeffectofGFAonINa,Lwasnotaffectedby200μmol·L-1H2O2.ItinhibitedIHERGwithanIC50of(273±34)μmol·L-1andhasslightblockingeffectonIKv1.5,decreasingIKv1.5byonly20.6%at200μmol·L-1.Insummary,GFAinhibitedINa.Lselectivelyandremainedsimilarinhibitioninpresenceofreactiveoxygenspecies..ThesefindingsmaysuggestanovelmolecularmechanismforthepotentialclinicalapplicationofGFAinthetreatmentofcardiovasculardisorders.

简介：介绍Cystone是为各种各样的尿混乱在印度使用的同意的Ayurvedicpolyherbal专卖药品，包括urolithiasis。试图在urolithiasis把Cystone的保护的效果与导致hyperoxaluria的氧化应力和钙盐水晶免职作比较。方法乙烯乙二醇(例如)(0.75%，V/V)在喝，水被给老鼠28天与Cystone(500和750mg/kg身体重量)的同时的处理导致urolithiasis，并且urolithiasis的各种各样的尿风险因素和抗氧化剂标记被估计。例如结果处理导致增加的尿体积和降低的尿pH与盐的增加的尿排泄一起，在未经治疗的动物的钙和磷酸盐。这些变化在未经治疗的老鼠的肾引起了广泛的钙盐水晶免职，增加的类脂化合物peroxidation和抗氧化剂酶(草皮，过氧化氢酶和GPx)的减少的活动。Cystone阻止了这些hyperoxaluric表明并且在两剂量在对待的老鼠禁止了钙盐水晶免职。结论Cystone治疗由改进肾的织物抗氧化剂地位和多尿对导致hyperoxaluria的氧化应力和钙盐水晶免职提供保护。

简介：Thepresentstudywasdesignedtosynthesize2-Cyano-3,12-dioxooleana-1,9(11)-en-28-oate-13β,28-olide(1),alactonederivativeofoleanolicacid(OA)andevaluateitsanti-inflammatoryactivity.Compound1significantlydiminishednitricoxide(NO)productionanddown-regulatedthemRNAexpressionofiNOS,COX-2,IL-6,IL-1β,andTNF-αinlipopolysaccharide(LPS)-stimulatedRAW264.7cells.FurtherinvivostudiesinmurinemodelofLPS-inducedacutelunginjury(ALI)showedthat1possessedmorepotentprotectiveeffectsthanthewell-knownanti-inflammatorydrugdexamethasonebyinhibitingmyeloperoxidase(MPO)activity,reducingtotalcellsandneutrophils,andsuppressinginflammatorycytokinesexpression,andthusamelioratingthehistopathologicalconditionsoftheinjuredlungtissue.Inconclusion,compound1couldbedevelopedasapromisinganti-inflammatoryagentforinterventionofLPS-inducedALI.