4-beta-phorbol 12-myristate 13-acetate (PMA), when administered topically to mouse ear, induces a pronounced inflammatory response mediated by protein kinase C (PKC). Activation of PKC is implicated in the pathogenesis of inflammation, with phospholipase A(2)-dependent arachidonic acid release and eicosanoid production. We have investigated the effects of hydroxyachillin, a sesquiterpene lactone from Tanacetum microphyllum DC., on mouse ear oedema induced by PMA. The effects of this compound on swelling and other inflammatory parameters are described. Hydroxyachillin significantly (p less than or equal to 0.01) inhibited ear swelling in a dose-dependent manner, and was as effective as the reference drugs. The PMA-induced vascular permeability was significantly (p less than or equal to 0.05) reduced by hydroxyachillin at the highest dose (3 mg/ear). Histologically, the signs of inflammation were greatly reduced in the hydroxyachillin-treated ear lesions. These data suggest that hydroxyachillin is an effective anti-inflammatory agent in this model, and that the inhibition of PKC may be one of the mechanisms of hydroxyachillin's effect.