Epigallocatechin-3-gallate suppresses the global interleukin-1beta-induced inflammatory response in human chondrocytes.docVIP

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Epigallocatechin-3-gallate suppresses the global interleukin-1beta-induced inflammatory response in human chondrocytes.doc

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Epigallocatechin-3-gallate suppresses the global interleukin-1beta-induced inflammatory response in human chondrocytes

AkhtarandHaqqiArthritisResearchTherapy2011,13:R93 /content/13/3/R93 RESEARCH ARTICLE OpenAccess Epigallocatechin-3-gallatesuppressestheglobal interleukin-1beta-inducedinflammatoryresponse inhumanchondrocytes NahidAkhtarandTariqMHaqqi* Abstract Introduction:Epigallocatechin-3-gallate(EGCG)isabioactivepolyphenolofgreenteaandexertspotentanti- inflammatoryeffectsbyinhibitingsignalingeventsandgeneexpression.Interleukin-1beta(IL-1b)istheprincipal cytokinelinkedtocartilagedegradationinosteoarthritis(OA).Theobjectiveofthisstudywastoevaluatethe globaleffectofEGCGonIL-1b-inducedexpressionofproteinsassociatedwithOApathogenesisinhuman chondrocytes. Methods:PrimaryOAchondrocyteswerepretreatedwithEGCG(10to100uM)andthenstimulatedwithIL-1b (5ng/ml)for24hours.Culturesupernatantswereincubatedwithcytokineantibodyarraysandimmunoreactive proteins(80proteins)werevisualizedbyenhancedchemiluminiscence.EffectofEGCGonIL-1b-inducedexpression of18selectedgeneswasverifiedbyRealtime-PCRandeffectonIL-6,IL-8andtumornecrosisfactor-alpha(TNF-a) productionwasdeterminedusingspecificELISAs.WesternimmunoblottingwasusedtoanalyzetheeffectofEGCG ontheinterleukin-1receptor-associatedkinase1(IRAK-1)andTNFreceptor-associatedfactor6(TRAF-6)proteinsin IL-1b-stimulatedchondrocytes.Theroleofnuclearfactorkappa-B(NF-B)andmitogenactivatedproteinkinases (MAPKs)intheregulationofselectedgenesandthemechanisminvolvedinEGCGmediatedmodulationofthese geneswasdeterminedbyusingspecificinhibitorsforNF-B(MG132)andMAPKs(p38-MAPK,SB202190;JNK- MAPK,SP600125,ERK-MAPK,PD98059). Results:Outof80proteinspresentonthearray,constitutiveexpressionof14%proteinswasalteredbyEGCG treatment.Nosignificantstimulatoryeffectwasobservedontheproteinsassociatedwithcartilageanabolic response.StimulationwithIL-1benhancedtheexpressionof29proteins.Expressionofall29proteinsup-regulated byIL-1bwasfoundtobesuppressedbyEGCG.EGCGalsoinhibitedtheexpressionofthesignalingintermediate TRAF-6at50and100uMconcentrations(P0.05).Ourresultsidentifiedseveralnewtarg