中医药SCI论文范本

ORIGINALARTICLETongxinluoInhibitsOxidizedLow-densityLipoprotein–inducedMaturationofHumanDendriticCellsviaActivatingPeroxisomeProliferator-ActivatedReceptorGammaPathwayWeiSu,PhD,*†AijunSun,MD,*‡DanlingXu,PhD,*HongqiZhang,PhD,*LinYang,PhD,*LingyanYuan,PhD,*JianguoJia,MS,*YunzengZou,MD,*‡YilingWu,MS,§KeqiangWang,MS,*andJunboGe,MD*‡Abstract:TongXinLuo(TXL)isatraditionalChineseherbalmedicinewithmultiplevasoprotectiveactivities.Dendriticcells(DCs)playanactiveroleintheimmunologicalprocessesrelatedtoatherosclerosis.ThepurposeofthisstudywastodeterminetheeffectandpossiblemechanismsofTXLonoxidizedlow-densitylipopro-tein(OX-LDL)–inducedmaturationandimmunefunctionofDCs.Humanmonocyte-derivedDCswereincubatedwithTXLorcigli-tazoneandweresubsequentlystimulatedwithOX-LDLtoinducematuration.Similartociglitazone,aperoxisomeproliferator-activatedreceptor(PPAR)gammaagonist,TXLcouldsignificantlyreducethematuration-associatedmarkersinducedbyOX-LDL,suchasCD40,CD86,CD1a,andhumanleukocyteantigen-DR;improvedtheendocytoticfunction;anddecreasedsecretionsofcytokinein-terleukin-12andtumornecrosisfactoralpha.TheseinhibitoryeffectsofTXLcouldbepartlyreversedbysilencingtheexpressionofPPARgammainDCs.Inconclusion,TXLcouldinhibitOX-LDL–inducedmaturationofDCsthroughactivatingPPARgammapathway.KeyWords:dendriticcells,atherosclerosis,oxidized-LDL,Tong-XinLuoextract(TXL)(JCardiovascPharmacolTM2010;56:177–183)INTRODUCTIONAtherosclerosishasbeenconsideredasyndromeofdysregulatedlipidstorageuntilrecentevidenceemphasizingthecriticalcontributionoftheimmunesystem.1Dendriticcells(DCs)arethemostpotentantigen-presentingcells.2DCsarepresentintheirimmatureformsinnondiseasedarteriesandbecomeactivatedduringatherogenesis.SomeDCsdirectlyclusterwithTcellswithinatheroscleroticlesions,whereasothersmigratetolymphoidorganstoactivateTcells.2DCspopulatinginatheroscleroticlesionsmightstimulateT-cellproliferationandinteractwithTcellstoregulateinnateimmunityinatherosclerosis.3InhibitingthematurationofDCsmaybebeneficialforthesuppressionofdamagingimmuneresponsesinatherosclerosis.4TongXinLuo(TXL)isamixtureoftraditionalChineseherbalmedicine(pharmacologicalinformationprovidedinSupplementalDigitalContents1and2(seeFigure1,://links.lww.com/JCVP/A19).Itisextracted,concentrated,andfreeze-driedfromagroupofherbalmedicines,suchasginseng,radixpaeoniaerubra,borneol,andspinyjujubaseed,whichcontainmultipleactivecomponentsthatmayberesponsibleforitsmultiplevasoprotectiveeffects.Inadouble-blindedclinicaltrial,Xuetal5evidencedsuperiorcurativeeffectonanginapectorisbyTXLcapsuletreatmentcomparedwiththecontrolgroup.Youetal6showedthattheroutinedrugplusTongxinluocapsulesismoreeffectiveonthereductionofinfarctionsizepost-reperfusionforthepatientswhosufferedfromacutemyocardialinfarction.Zhangetal7andLietal8reportedthatTXLdoesdependentlyenhancedthestabilityofvulnerableplaquesandpreventedplaquesfromruptureinaorticatherosclerosisrabbitmodelsviainhibitingtheexpressionofcyclooxygenase-2andmatrixmetalloproteinase(MMP).IncreasingevidencealsosuggestedthatDCsmightplayanactiveroleintheimmunologicalprocessesleadingtoatherosclerosis.3,4We,therefore,testedthehypothesisthattheantiatheroscleroticeffectsofTXLcouldbemediatedbymodulatingDCmaturationinthepresentstudy.Inthisstudy,weanalyzedtheexpressionofmaturationmarkerssuchasCD40,CD1a,CD86,andhumanleukocyteantigen-DR(HLA-DR);theendocytoticability;andtheReceivedforpublicationMarch3,2010;acceptedMay3,2010.Fromthe*ShanghaiInstituteofCardiovascularDiseases,ZhongshanHospital,FudanUniversity,Shanghai,China;†DepartmentofPathology,XinXiangMedicalUniversity,HeNan,China;‡InstituteofBiomedicalScience,FudanUniversity,Shanghai,China;and§TheIntegrationofTraditionalandWesternMedicalResearchAcademyofHebeiProvince,Shijiazhuang,China.W.SuandA.Sunhavecontributedequallytothiswork.SupportedbyNationalBasicResearchProgramofChina(2005CB523302and2006CB503803),863ProgramofScienceandTechnologyMinistry(2006AA0ZA406),andOutstandingYouthGrantfromNationalNaturalScienceFoundationofChina(30725036).Disclosure:Therearenofinancialorotherrelationsthatcouldleadtoaconflictofinterest.Reprints:JunboGe,MD,ShanghaiInstituteofCardiovascularDiseases,ZhongshanHospital,FudanUniversity,180FenglinRd,Shanghai,200032,People’sRepublicofChina(e-mail:[e-mail]).Supplementaldigitalcontentsareavailableforthisarticle.DirectURLcitationsappearintheprintedtextandareprovidedintheHTMLandPDFversionsofthisarticleonthejournal’sWebsite().Copyright
2010byLippincottWilliams&WilkinsJCardiovascPharmacol
Volume56,Number2,August2010|177secretionsofcytokineinDCstreatedwithoxidizedlow-densitylipoprotein(OX-LDL)intheabsenceandpresenceofTXLorciglitazone.Theexpressionofperoxisomeproliferator-activatedreceptor(PPAR)-gwasknockeddownonculturedDCsbysmallinterferingRNA(siRNA)todeterminethepotentialmechanismsofTXLoninhibitingthematurationofDCs.MATERIALSANDMETHODSAntibodies,Proteins,andReagentsFluoresceinisothiocyanate(FITC)–labeledorphycoer-ythrin-labeledantibodiestohumanCD40,CD86