Research Information System
EUROPEAN JOURNAL OF PHARMACOLOGY, vol.506, no.2, pp.189-197, 2004 (SCI-Expanded)
To investigate a possible role of 8-isoprostaglandin F-2alpha in inflammation, 8-isoprostaglandin F-2alpha and prostaglandin E-2 levels were determined by enzyme immunoassay (EIA) in carrageenan-induced air pouch model in rats. In this model, 8-isoprostaglandin F-2alpha and prostaglandin E-2 levels were found to be increased significantly. To evaluate whether this increase was due to the development of inflammation or solely to cyclooxygenase-2 induction, a lipopolysaccharide-induced air pouch model, in which only cyclooxygenase-2 induction occurs without inflammation, was used. In this model, 8-isoprostaglandin F-2alpha was also found to be increased parallel to the increase in prostaglandin E-2 level. Cyclooxygenase-dependent formation of 8-isoprostaglandin F-2alpha was investigated in carrageenan-induced air pouch model by administrating nonselective cyclooxygenase inhibitor indomethacin, selective cyclooxygenase-1 inhibitor valeryl salicylate or selective cyclooxygenase-2 inhibitor SC-582368 (4-(5-(4-chlorophenyl)-3-3-trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonanmide) 1 h before carrageenan injection. All these inhibitors significantly inhibited the production of 8-isoprostaglandin F-2alpha and prostaglandin E-2. These findings show that 8-isoprostaglandin F-2alpha can be formed in carrageenan-induced air pouch model in rats. The formation of 8-isoprostaglandin F-2alpha in lipopolysaccharide-induced air pouch model and the inhibition of its production by various cyclooxygenase inhibitors provide evidence for cyclooxygenase-dependent fort-nation of isoprostanes in this model. (C) 2004 Elsevier B.V. All rights reserved.