Difference in reduction of endogenous prostaglandin E₂ and prostacyclin levels in rat gastric mucosa between pranoprofen and indomethacin

Abstract

Non-steroidal antiinflammatory drugs (NSAID) produce the acute gastric mucosal lesions in relation to the inhibition of prostaglandin (PG) biosynthesis in animals and humans. We tested the effect of pranoprofen and indomethacin on gastric mucosal damage and mucosal PGE₂ and prostacyclin (PGI₂) levels in a same antiinflammatory dose (ED₅₀ on the carrageenin-induced foot edema) in rats. The animals were intragastrically given pranoprofen three times before sacrifice in a dose of 0.58 mg/kg or indomethacin in a dose of 3.8 mg/kg. Endogenous PGE₂ and PGI₂ in fundic mucosa were determined by radioimmunoassay. Pranoprofen is less potent than indomethacin to produce the gastric mucosal lesions. The PG levels were not reduced in rats given pranoprofen but were markedly reduced in rats given indomethacin. These results suggest that the ulcerogenicity of pranoprofen is less potent than indomethacin, and this difference may be related to the PG levels in rat gastric mucosa.