Article
Anti-inflammatory effects of carvacrol: evidence for a key role of interleukin-10.
Registro en:
LIMA, M. S. et al. Anti-inflammatory effects of carvacrol: evidence for a key role of interleukin-10. European Journal of Pharmacology, v. 699, n. 1-3, p. 112-117, 2013.
1879-0712
10.1016/j.ejphar.2012.11.040
Autor
Lima, Milena da Silva
Quintans Junior, Lucindo José
Santana, Wagno Alcântara
Kaneto, Carla Martins
Soares, Milena Botelho Pereira
Villarreal, Cristiane Flora
Resumen
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.