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：目的methotrexate(MTX)的最重要的副作用是mucositis。这研究的目的是在收到methotrexate的老鼠在肠的损坏和氧化应力上评估沉金摘录的效果。方法实验在划分成六个组的男Wistar白化体老鼠上被执行。首先组织收到的正常盐口头上地，第二个组收到了沉金摘录(100mg瑡潩?????????????????假吗？？

简介：作为一个内部应用的反煽动性的代理人，Escin广泛地在从损伤或操作导致诊所的发炎和浮肿的治疗被使用了。然而，它皮肤的发炎和浮肿上的外部使用的效果仍然保持未经勘探。在现在的学习，反煽动性并且escin的外部使用的anti-edematous效果在老鼠，在老鼠胀大的导致paraxylene的耳朵，和棉花在导致carrageenan的爪浮肿和导致组织安的毛状的渗透被学习在老鼠的导致小团的granuloma。前列腺素E2(PGE2)上的escin胶化的外部使用的效果，肿瘤坏死因素--(TNF-)，并且interleukin-1(IL-1)被ELISA决定。反煽动性的机制被与西方的弄污和实时PCR分析检测glucocorticoid受体(GR)的表示探索，与原子factor-B(NF-B)的进一步的探索，p38激活mitogen的蛋白质kinase(P38MAPK)和使活跃之物protein-1(AP-1)表情。我们证明escin的外部使用证明在不同动物模型的尖锐、长期的发炎上的重要反煽动性的效果和它的反煽动性的效果可能与PGE2，TNF-，和IL-1的下面规定有关。结果也证明escin由支持GR的表示施加了它的反煽动性的效果，与是的可能的机制象NF-B和AP-1那样的GR相关的发信号的分子的表情的抑制。

简介：

简介：在hematological上调查Ipomoeacarnea花的乙醇摘录的活跃氯仿部分的目的在Wistar老鼠在甲苯改变导致diisocyanate的发炎。方法除了控制组，，所有用10%甲苯diisocyanate(TDI)的5L的intranasal申请老鼠被敏化7天。在第二促进感受性以后的一个星期，所有与5%TDI的5L老鼠被挑起导致航线超敏性。在最后挑战以后，血和bronchoalvelorlavage(BAL)液体镇定、使遭到总计，微分白细胞数。闪光层析在最活跃的氯仿部分上被执行孤立一个单个部件。有在200mg摥琠敨洠獯?汰畡楳汢?潳牵散漠?畨慭?湩敦瑣潩?的口头的剂量的ethanolic摘录和它的氯仿部分的结果处理??桴?慳敭瀠牥潩?挠獡獥漠?L牯楴湯挠畡敳?祢??畢湲瑥楩眠牥?潣普物敭?瑡琠潷搠楡祲猠敨灥映牡獭?匊湩散㈠??愠氠牡敧洠汵楴楤'諡箻H慮祲爠獥慥捲?潰瑲潦楬?慨?瑳牡整?愠浩摥愠?敧敮慲楴杮戠瑥整?湫睯敬杤?L畯?桴獩搠獩慥敳?湉?湵?????敦敶?湩猠慭汬爠浵湩湡獴欠灥?潦?業歬瀠潲畤瑣潩?敢慣敭渠瑯晩慩汢?湩琠敨丠瑥敨汲湡獤映牯映牡獭眠瑩?湡愠潢瑲潩?慲整漠?潭敲琠慨?楦敶瀠牥挠湥???桴?畡畴湭漠

简介：Cisplatinandotherplatinum-baseddrugsareusedfrequentlyfortreatmentoflungcancer.However,theirclinicalperformanceareusuallylimitedbydrugresistanceortoxiceffects.Carnosicacid,apolyphenolicditerpeneisolatedfromRosemary(Rosemarinusofficinalis),hasbeenreportedtohaveseveralpharmacologicalandbiologicalactivities.Inthepresentstudy,thecombinationeffectofcisplatinpluscarnosicacidonmouseLLC(Lewislungcancer)xenograftsandpossibleunderlyingmechanismofactionwereexamined.LLC-bearingmiceweretreatedwithintraperitonealinjectionwithcisplatin,oralgavagewithcarnosicacid,orcombinationwithcisplatinandcarnosicacid,respectively.Combinationofcarnosicacidandcisplatinyieldedsignificantlybetteranti-growthandpro-apoptoticeffectsonLLCxenograftsthandrugsalone.MechanisticstudyshowedthatcarnosicacidtreatmentboostedthefunctionofCD8~+TcellsasevidencedbyhigherIFN-γsecretionandhigherexpressionofFasL,perforinaswellasgranzymeB.Inthemeantime,theproportionofMDSC(myeloid-derivedsuppressorcells)intumortissueswerereducedbycarnosicacidtreatmentandthemRNAlevelsofiNOS2,Arg-1,andMMP9,whicharethefunctionalmarkersforMDSC,werereduced.Inconclusion,ourstudyprovedthatthefunctionalsuppressionofMDSCbycarnosicacidpromotedthelethalityofCD8~+Tcells,whichcontributedtotheenhancementofanti-lungcancereffectofcisplatin.

简介：ThisstudydevelopedapopulationpharmacokineticmodelforsodiumtanshinoneIIAsulfonate(STS)inhealthyvolunteersandcoronaryheartdisease(CHD)patientsinordertoidentifysignificantcovariatesforthepharmacokineticsofSTS.Bloodsampleswereobtainedbyintensesamplingapproachfrom10healthyvolunteersandsparsesamplingfrom25CHDpatients,andapopulationpharmacokineticanalysiswasperformedbynonlinearmixed-effectmodeling.Thefinalmodelwasevaluatedbybootstrapandvisualpredictivecheck.Atotalof230plasmaconcentrationswereincluded,137fromhealthyvolunteersand93fromCHDpatients.Itwasatwo-compartmentmodelwithfirst-orderelimination.Thetypicalvalueoftheapparentclearance(CL)ofSTSinCHDpatientswithtotalbilirubin(TBIL)levelof10μmol(L?1was48.7L(h?1withinterindividualvariabilityof27.4%,whereasthatinhealthyvolunteerswiththesameTBILlevelwas63.1L(h?1.Residualvariabilitywasdescribedbyaproportionalerrormodelandestimatedat5.2%.TheCLofSTSinCHDpatientswaslowerthanthatinhealthyvolunteersanddecreasedwhenTBILlevelsincreased.Thebootstrapandvisualpredictivecheckconfirmedthestabilityandvalidityofthefinalmodel.TheseresultssuggestedthatSTSdosageadjustmentmightbeconsideredbasedonTBILlevelsinCHDpatients.

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简介：Notopterygiumincisum(QH)hasbeenusedforthetreatmentofrheumatoidarthritis(RA),andvolatileoilsmaybeitsmainlybioactiveconstituents.ThepresentstudywasdesignedtoanalyzethevolatilecompoundsinQHandtodeterminetheanti-arthriticcapacityofNotopterygiumvolatileoilsandthepotentialmechanismofaction.ThevolatilecompoundsanalysiswasconductedbyGC-MS.Theanti-arthriticcapacitytestofthevolatileoilswasconductedonadjuvant-inducedarthritis(AIA)rats.Theanti-inflammatorypropertywastestedinNOreleasemodelinRAW264.7cells.Endothelialcellswereusedtoevaluatetheanti-proliferativeandanti-tubeformativeeffects.70compoundswereanalyzedbyGC-MSinthevolatileoils.NotopterygiumvolatileoilsweakenedtheratAIAinadose-dependentmanner(2,4,and8gcrudedrug/kg).TheNOproductionbyRAW264.7wasdecreasedbymorethan50%inNotopterygiumvolatileoils(5,15,and45μg·mL-1)pretreatedgroups.NotopterygiumvolatileoilsalsoinhibitedEAhy926cellproliferationandfurtherdelayedEAhy926cellcapillarytubeformationinaconcentration-dependentmanner.Theanti-NOproductive,anti-proliferative,andanti-tubeformativeeffectsofNotopterygiumvolatileoilsstronglysuggestedthatthetherapeuticeffectofQHinAIAmightberelatedtothepotentanti-inflammatoryandanti-angiogeniccapacitiesofthevolatileoils.

简介：Capsaicin(trans-8-methyl-N-vanillyl-6-nonenamide)isthemaincomponentinhotpeppers,includingredchilipeppers,alapenos,andhabanero,belongingtothegenusCapsicum.Capsaicinisapotentantioxidantthatinterfereswithfreeradicalactivities.Inthepresentstudy,thepossibleprotectiveeffectofcapsaicinwasstudiedagainstmethylmethanesulphonate(MMS)inducedtoxicityinthirdinstarlarvaeoftransgenicDrosophilamelanogaster(hsp70-lacZ)Bg~9.ThethirdinstarwasallowedtofeedonthediethavingdifferentdosesofcapsaicinandMMSseparatelyandincombination.TheresultssuggestedthattheexposureofthirdinstarlarvaetothediethavingMMSaloneshowedsignificanthsp70expressionaswellastissueDNAandoxidativedamage,whereasthelarvaefeedonthediethavingMMSandcapsaicinshowedadecreaseinthetoxiceffectsfor48-hofexposure.Inconclusion,capsaicinshowedadose-dependentdecreaseinthetoxiceffectsinducedbyMMSinthethirdinstarlarvaeoftransgenicDrosophilamelanogaster.