Carvacrol is a phenolic
monoterpene present in the
essential oil of the family Lamiaceae, as in the genera Origanum and Thymus. We previously reported that
carvacrol is effective as an
analgesic compound in various nociceptive models, probably by inhibition of peripheral mediators that could be related with its strong
antioxidant effect observed in vitro. In this study, the anti-hypernociceptive activity of
carvacrol was tested in mice through models of mechanical hypernociception induced by
carrageenan, and the involvement of important mediators of its signaling cascade, as
tumor necrosis factor-alpha (TNF-α),
prostaglandin E(2) (
PGE(2)), and
dopamine, were assessed. We also investigated the anti-inflammatory effect of
carvacrol on the model of
carrageenan-induced
pleurisy and mouse paw
edema, and the
lipopolysaccharide (LPS)-induced
nitrite production in murine macrophages was observed. Systemic pretreatment with
carvacrol (50 or 100 mg/kg; i.p.) inhibited the development of mechanical hypernociception and
edema induced by
carrageenan and TNF-α; however, no effect was observed on hypernociception induced by
PGE(2) and
dopamine. Besides this,
carvacrol significantly decreased TNF-α levels in pleural lavage and suppressed the recruitment of leukocytes without altering the morphological profile of these cells.
Carvacrol (1, 10, and 100 μg/mL) also significantly reduced (p < 0.001) the LPS-induced
nitrite production in vitro and did not produce citotoxicity in the murine peritoneal macrophages in vitro. The spontaneous locomotor activity of mice was not affected by
carvacrol. This study adds information about the beneficial effects of
carvacrol on mechanical hypernociception and
inflammation. It also indicates that this
monoterpene might be potentially interesting in the development of novel tools for management and/or treatment of painful conditions, including those related to inflammatory and prooxidant states.