The Secret For CASK

01) by carvacrol at 100?mg/kg ( Fig. 3C and A, respectively). The kinetics of IL-1�� production showed that the inhibitory effects of carvacrol persisted until 24?h after CFA challenge ( Fig. 3D). As expected, the pretreatment with dexamethasone (2?mg/kg, i.p.) reduced the production of TNF-�� and IL-1�� induced by CFA ( Fig. 3; PJAK inhibitor (50 and 100?mg/kg) or dexamethasone (0.5?mg/kg) had a significant (PMAPK inhibitor ( Fig. 2D). Similarly, the local production of IL-10 ( Fig. 3E) was enhanced by carvacrol at 50?mg/kg (PCASK and PGE2 levels and the induction of COX-2 expression. In addition, carvacrol enhanced the local IL-10 release, while was unable to reduce the inflammation in IL-10 knockout mice. Therefore, the present data suggest that carvacrol induces anti-inflammatory effects by reducing the production of IL-1�� and PGE2, important inflammatory mediators, possible through a mechanism dependent on IL-10 production. Using an experimental protocol for screening of new anti-inflammatory drugs, the CFA-induced paw inflammation model, the mechanisms involved with the anti-inflammatory action of carvacrol were investigated. Administration of carvacrol reduced the CFA-induced paw edema, confirming the data from Guimar?es et al. (2012) showing that carvacrol has anti-edematogenic properties in mice. In fact, the anti-inflammatory activity of carvacrol has been demonstrated by in vitro and in vivo assays (Botelho et al., 2009, Hotta et al., 2010, Landa et al., 2009?and?Wagner et al., 1986). CFA, which consists of heat-killed mycobacteria suspended in a mineral oil vehicle, produces a chronic inflammatory condition when injected into rodents.