简介:Chemokinesbelongtoalargefamilyofinflammatorycytokinesresponsibleformigrationandaccumulationofleukocytesatinflammatorysites.Overthepastdecade,accumulatingevidenceindicatedacrucialroleforchemokinesandchemokinereceptorsinthepathophysiologyofrheumatoidarthritis(RA).RAisachronicautoimmunediseaseinwhichthesynovialtissueisheavilyinfiltratedbyleukocytes.Chemokinesplayanimportantroleintheinfiltration,localization,retentionofinfiltratingleukocytesandgenerationofectopicgerminalcentersintheinflamedsynovium.RecentevidencealsosuggeststhatidentificationofinhibitorsdirectlytargetingchemokinesortheirreceptorsmayprovideanoveltherapeuticstrategyinRA.TraditionalChinesemedicinals(TCMs)havealonghistoryinthetreatmentofinflammatoryjointdisease.ThebasisfortheclinicalbenefitsofTCMremainslargelyunclear.Ourstudieshaveledtotheidentificationofnumerousnovelchemokine/chemokinereceptorinhibitorspresentinanti-inflammatoryTCMs.Alloftheseinhibitorswerepreviouslyreportedbyotherresearcherstohaveanti-arthriticeffect,whichmaybeattributable,atleastinpart,totheirinhibitoryeffectonchemokineand/orchemokinereceptor.Therefore,identificationofagentscapableoftargetingchemokine/chemokinereceptorinteractionshassuggestedamechanismofactionforseveralTCMcomponentsandprovidedameansofidentifyingadditionalanti-RATCM.Thus,thisapproachmayleadtothediscoveryofnewinhibitorsofchemokinesorchemokinereceptorsthatcanbeusedtotreatdiseasesassociatedwithinappropriatelyoveractivechemokinemediatedinflammatoryreactions.Cellular&MolecularImmunology.2004;1(5):336-342.
简介:目的观察PS-1突变型L286V对RA诱导的PC12细胞生长和凋亡的影响.方法运用脂质体介导的基因转染技术建立稳定表达PS-1WT和突变型L286V基因的细胞克隆,采用MTT法、流式细胞仪检测细胞生长曲线、生长周期及细胞凋亡情况.结果(1)PS-1突变型L286V能使RA诱导的PC12细胞增殖指数降低,G1期细胞增多、S期细胞减少;(2)在正常培养条件和无血清培养下,PS-1突变型L286V对RA诱导的PC12细胞均具有促进细胞凋亡的作用,以无血清培养时表现得更为明显.结论PS-1突变型L286V对RA诱导的PC12细胞生长具有抑制作用和促进细胞凋亡的作用.
简介:BasedonageneralanalysisofGreenfunctionsinthereal-timethermalfieldtheory,wehaveproventhatthefour-pointamputatedfunctionsinanNJLmodelinthefermionbubblediagramapproximationbehavelikeusualtwo-pointfunctions.WeexpoundthethermaltransformationsofthematrixpropagatorsforascalarboundstateintheFFbasisandintheRAbasisrespectively.Theresultingphysicalcausal,advancedandretardedpropagatorsarerespectivelyidenticaltocorrespondingonesderivedintheimaginary-timeformalism,andthisshowsonceagainthecompleteequivalenceofthetwoformalismsofthermalfieldtheoryonthediscussedproblemintheNJLmodel.
简介:中药现代化是中药迈向世界尤为重要的一步。本研究运用经典RA动物模型,结合现代分子生物学,以免疫组织化学、生化等方法,深入探讨其对类风湿性关节炎模型血清神经递质的影响,并从分子水平上观察其对实验性RA大鼠模型血清中IL-1β、TNFα、VEGF等细胞因子含量的调控、对神经内分泌网络的调控的影响。结果表明:1.金骨莲胶囊能显著降低实验性RA大鼠血清中5-HTP、5-HIAA含量;2.金骨莲胶囊能明显抑制实验性RA大鼠免疫系统分泌IL-1β、TNFα、VEGF等细胞因子,降低IL-1β、TNFα、VEGF在血清中的含量;3.金骨莲胶囊能明显上调实验性RA大鼠血清中Cor的含量。