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1、ChineseJournalofNaturalChineseJournalofNaturalMedicines2012,10(2):0142−0149Medicinesdoi:10.3724/SP.J.1009.2012.00142Diosgeninreducesleukocytesadhesionandmigrationlinkedwithinhibitionofintercellularadhesionmolecule-1expres-sionandNF-κBp65activationinendothelialcells1,2a1,21,2*1,2*SONGJia
2、-Xi,MALi,KOUJun-Ping,YUBo-Yang1DepartmentofComplexPrescriptionofTCM,ChinaPharmaceuticalUniversity,Nanjing211198,China;2StateKeyLaboratoryofNaturalMedicines,ChinaPharmaceuticalUniversity,Nanjing210009,ChinaAvailableonline20Mar.2012[ABSTRACT]AIM:Toinvestigatetheanti-inflammatoryactivityan
3、dpossiblemechanismofdiosgenin,andtoprovidesomefurtherpharmacologicalevidenceforitsclinicalapplications.METHODS:Anti-inflammatoryactivitiesofdiosgeninwereevaluatedbyzy-mosanA–evokedperitonealleukocytesmigrationinmiceandtheadhesionofhumanpro-myelocyticleukemiacellstrain(HL-60)tohumanumbil
4、icalveinendothelialcellline(ECV304)cellsinducedbytumornecrosisfactor(TNF-α).Furthermore,theeffectsofdiosgeninonTNF-α–inducedintercellularadhesionmolecule-1(ICAM-1)expressionwerealsoinvestigatedbyreversetranscrip-tion-PCR(RT-PCR)andflowcytometricanalysis,andnuclearfactor-kappaB(NF-κB)/p6
5、5translocationandphosphorylationweredeterminedbyWesternblot.RESULTS:DiosgeninsignificantlyinhibitedperitonealleukocytesmigrationinducedbyzymosanAin−1micewhengivenorallyonceatdosesof1and3mg·kg.PretreatmentECV304cellswithdiosgeninatconcentrationsof0.1and1−1μmol·Lfor5hremarkablydecreasedTN
6、F-α-stimulatedadhesionofHL-60toECV304cellsinvitro,withnoeffectonviabilityofECV304cells.Furthermore,diosgenininhibitedTNF-α–inducedoverexpressionofICAM-1bothatthemRNAandproteinlevels,andsuppressednuclearp65accumulationandp65activationinECV304cells.CONCLUSION:Theseresultssuggestedthatdios
7、geninsignificantlyinhibitedleukocytesmigrationandadhesion,partlyduetothedown-regulationofICAM-1expressionthroughNF-κBpath-way.[KEYWORDS]Diosgenin;Leukocytesadhesionandmigration;Intercellularadhesionmolecule-1;Nuclearfactor-kappaB[CLCNumber]R965[Documentcode]A[ArticleID]1672-365