Role of prostaglandin E2 on gastric ulcers induced by non-steroidal anti-inflammatory compounds (NOSAC).
We investigated the effect of indomethacin and aspirin on the prostaglandin E2 (PGE2) levels in rat gastric mucosa. In untreated controls, the PGE2 level was 1085 +/- 80 ng/g in the fundic- and 2435 +/- 339 ng/g in the antral mucosa; it was markedly reduced by indomethacin (6 or 20 mg/kg) in a dose-related manner prior to the formation of gastric ulcers. Aspirin (200 mg/kg) also decreased the mucosal PGE2 content. The simultaneous infusion of 5 microgram/kg 16, 16-dimethyl PGE2 and 20 mg/kg indomethacin inhibited the formation of gastric ulcers. Our experimental results suggested that the indomethacin- or aspirin-induced gastric mucosal lesions are due to a deficiency of endogenous mucosal PGE2.
D000818:Animals; D001241:Aspirin / Q000009:adverse effects*; D015232:Dinoprostone; D005753:Gastric Mucosa / Q000032:analysis; D007213:Indomethacin / Q000009:adverse effects*; D008297:Male; D011458:Prostaglandins E / Q000494:pharmacology / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000139:chemically induced*
D011458:Prostaglandins E; D015232:Dinoprostone; D001241:Aspirin; D007213:Indomethacin