Carvacrol,aphenolicmonoterpene,hasbeenreportedtopossessanti-inflammatoryproperties. However,themechanismsinvolvedinitspharmacologicalpropertiesarecurrentlynotwellunder- stood. Inthepresentstudy,thecontributionofcytokinemodulationtotheanti-inflammatoryeffectsof carvacrolwasinvestigatedinaclassicalinflammationmodel:thecompleteFreund’sadjuvant(CFA)- inducedpawinflammationinmice.Thepawedemawasmeasuredusingaplesthismometer.Pawtissue was removed2haftertheinflammatorystimulustodeterminethelevelsofprostaglandinE2 (PGE2) by enzyme immunoassay,thelevelsofinterleukin-1 b (IL-1b), tumornecrosisfactor-a (TNF-a), and interleukin-10(IL-10)byELISAorthemRNAexpressionofcyclooxygenase-2(COX-2),IL-1b, TNF-a, and IL-10 byreal-timePCR.Administrationofcarvacrolproducedanti-inflammatoryeffectsagainstCFA- inducedinflammationinmice.Treatmentofmicewithcarvacrolat50and100mg/kgattenuatedthe paw edemaandreducedtheIL-1b and PGE2, butnotTNF-a, locallevels.Similarly,carvacrol(100mg/kg) reducedtheCOX-2andIL-1b mRNA expression.ThelevelsofIL-10,ananti-inflammatorycytokine,and the IL-10mRNAexpressionintheinflamedpawwereenhancedbycarvacrol.Inaddition,thetreatment with carvacroldidnotreducetheCFA-inducedpawedemainIL-10knockoutmice.Thepresentresults suggestthatcarvacrolcausesanti-inflammatoryeffectsbyreducingtheproductionofinflammatory mediators,suchasIL-1b and prostanoids,possiblythroughtheinductionofIL-10release.