Effect of prostaglandin synthesis inhibitors on neurotensin and sodium salicylate-induced gastric cytoprotection in rats |
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Authors: | J E Adcock D E Hernandez C B Nemeroff A J Prange |
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Affiliation: | 1. Biological Sciences Research Center, University of North Carolina School of Medicine Chapel Hill, N.C. 27514, USA;2. Department of Psychiatry, University of North Carolina School of Medicine Chapel Hill, N.C. 27514, USA;3. Neurobiology Program, University of North Carolina School of Medicine Chapel Hill, N.C. 27514, USA |
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Abstract: | Sodium salicylate (SA) has been reported to inhibit the formation of gastric ulcerations induced by aspirin, indomethacin, and absolute ethanol. In this study, SA dose-dependently inhibited gastric ulcers induced by three hours of cold-restraint stress (CRS); SA-induced cytoprotection was prevented by both acetylsalicylic acid (aspirin) and indomethacin pretreatment. Neurotensin (NT), which has previously been demonstrated to prevent the development of CRS-induced gastric ulcerations after intracisternal administration, was found to be ineffective in animals pre-treated with aspirin, and with indomethacin, as previously described. These data suggest that in the CRS model both NT- and SA-induced gastric cytoprotection require a functionally intact gastrointestinal prostaglandin synthetic pathway. |
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