Effects of alminoprofen on sodium urate crystal-induced inflammation

Abstract

Effects of alminoprofen (AP), a non-steroidal anti-inflammatory agent, were investigated using several experimental gouty models. AP (3 ?? 30 mg/kg, p.o.) dose-dependently inhibited urate crystal-induced rat paw edema. AP (3 ?? 30 mg/kg, p.o.) inhibited the accumulation of exudate and decreased the total counts of leukocytes and the amount of PGE₂ in a dose-dependent manner in sodium urate crystalinduced pleuritic rats. AP (0.3 ?? 10 mg/kg, p.o.) showed a dose-related analgesic activity on the pain response in sodium urate crystal-induced arthritic rats. AP (10^-5 ?? 10^-3M) inhibited the sodium urate crystal-induced β-glucuronidase release from guinea pig neutrophils at more than 10^-4M. AP (10^-5 ?? 10^-3M) did not inhibit the sodium urate crystal-induced production of O₂^- from guinea-pig neutrophils. AP (10^-6 ?? 10^-4M) inhibited dose-dependently the chemotaxis of leukocytes induced by chemotactic factors from guinea pig neutrophils stimulated with sodium urate crystals. AP (10^-6 ?? 10^-4M) inhibited the sodium urate crystal-induced production of PGE₂ from rat peritoneal leukocytes in a dose-related manner. These results suggest that AP has a potent anti-inflammatory and analgesic activity in sodium urate crystal-induced inflammations, and these effects are exerted through its combined inhibitions of PGE₂ synthesis, leukocyte chemotaxis and lysosomal enzyme release.