Carvacrol, a phenolic
monoterpene, has been reported to possess anti-inflammatory properties. However, the mechanisms involved in its pharmacological properties are currently not well understood. In the present study, the contribution of
cytokine modulation to the anti-inflammatory effects of
carvacrol was investigated in a classical
inflammation model: the complete
Freund's adjuvant (CFA)-induced paw
inflammation in mice. The paw
edema was measured using a plesthismometer. Paw tissue was removed 2h after the inflammatory stimulus to determine the levels of
prostaglandin E(2) (
PGE(2)) by
enzyme immunoassay, the levels of
interleukin-1 β (IL-1β),
tumor necrosis factor-α (TNF-α), and
interleukin-10 (IL-10) by ELISA or the
mRNA expression of
cyclooxygenase-2 (COX-2), IL-1β, TNF-α, and
IL-10 by real-time PCR. Administration of
carvacrol produced anti-inflammatory effects against CFA-induced
inflammation in mice. Treatment of mice with
carvacrol at 50 and 100mg/kg attenuated the paw
edema and reduced the IL-1β and
PGE(2), but not TNF-α, local levels. Similarly,
carvacrol (100mg/kg) reduced the COX-2 and IL-1β
mRNA expression. The levels of
IL-10, an anti-inflammatory
cytokine, and the
IL-10 mRNA expression in the inflamed paw were enhanced by
carvacrol. In addition, the treatment with
carvacrol did not reduce the CFA-induced paw
edema in
IL-10 knockout mice. The present results suggest that
carvacrol causes anti-inflammatory effects by reducing the production of inflammatory mediators, such as IL-1β and
prostanoids, possibly through the induction of
IL-10 release.