Abstract
1 The inhibitory action of sulphasalazine on ethanol-induced gastric damage was studied in rats. 2 Sulphasalazine (62.5 or 125 mg kg-1, s.c.) did not affect basal gastric acid secretion but increased pepsin output. 3 Ethanol (40% v/v, 10 ml kg-1, p.o.) produced severe gastric glandular mucosal damage and lessened the stomach emptying rate of resin pellets, but it increased the levels of prostaglandin E2 (PGE2)-like activity in the glandular mucosa. 4 Sulphasalazine markedly prevented ethanol-induced damage and significantly elevated gastric wall mucus levels both in basal conditions and in the presence of ethanol. 5 Sulphasalazine caused a small insignificant increase in mucosal PGE2 levels in both control and ethanol-treated rats. The drug significantly increased mucosal PGE2 levels in indomethacin-treated animals, but did not prevent indomethacin-induced mucosal damage. 6 Sulphapyridine but not 5-aminosalicylic acid, constituents of sulphasalazine, showed a similar antilesion action to the parent drug, and prevented gastric wall mucus depletion in ethanol-treated animals. 7 This study elucidates the protective effects of sulphasalazine against ethanol-induced gastric lesions. The antagonistic action appears to be mediated, at least partly, through the preservation of gastric wall mucus by sulphapyridine.
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