Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D00446 (Sucralfate)
 278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study evaluated the effect of sucralfate and its components, sucrose octasulfate and aluminum hydroxide, on: (1) damage to rat cultured gastric mucosal cells induced by sodium taurocholate in a neutral environment and in conditions independent of systemic factors, (2) prostaglandin E2 and on 6-keto prostaglandin F1 alpha release by cultured cells, and (3) sulfhydryl content of cultured cells. Cell damage was quantitated by chromium-51 release assay. Prostaglandin E2 and 6-keto prostaglandin F1 alpha were measured by radioimmunoassay. Total sulfhydryl content of cultured cells was determined calorimetrically. Microscopically, sucralfate was found to adhere tightly to epithelial cell surfaces despite frequent washings. Sucralfate 2 mg/ml and 5 mg/ml significantly decreased taurocholate-induced damage, reducing taurocholate-induced specific 51Cr release by 11.8 points (equal to 29% decrease in cell damage, P less than 0.01) and 22.9 points (equal to 56% decrease in cell damage, P less than 0.001), respectively. Sucrose octasulfate and aluminum hydroxide did not exert significant protection against damage induced by sodium taurocholate. The protective effect of sucralfate was not prevented by indomethacin, nor was it counteracted by the sulfhydryl blocker, iodoacetamide. Sucralfate, but not its components, significantly and dose-dependently stimulated prostaglandin E2 (r = 0.94, P less than 0.05) and 6-keto prostaglandin F1 alpha (r = 0.89, P less than 0.05) production by cultured cells. Neither sucralfate nor its components affected sulfhydryl content of cultured cells. In conclusion, sucralfate, but not its components, (1) protects rat gastric mucosal cells against taurocholate-induced damage in conditions independent of systemic factors and in a neutral environment and (2) significantly stimulates prostaglandin production by cultured cells. (3) The protection by sucralfate in vitro does not seem to depend on its stimulatory effect on endogenous prostaglandin synthesis.
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PMID:Effect of sucralfate and its components on taurocholate-induced damage to rat gastric mucosal cells in tissue culture. 231 93

To assess the gastric mucosal protective action of sucralfate against alcohol, a double-blind, controlled, randomized study was carried out in 12 healthy adult men. All subjects received four treatments in a random sequence: sucralfate + ethanol, sucralfate + ethanol placebo, sucralfate placebo + ethanol, and sucralfate placebo + ethanol placebo. Fundal, antral, and duodenal mucosae were submitted to endoscopic examinations, and the antral mucosa underwent histologic examination before and after injury. Biopsy specimens were taken from the antral mucosa to determine by radioimmunoassay its capacity to synthesize prostaglandin E2, thromboxane B2, and 6-keto prostaglandin F1 alpha. In both the fundus and the antrum, the mean endoscopic injury score after sucralfate plus ethanol administration was significantly lower than that after ethanol alone. All treatments tended to increase prostanoid values but 6-keto prostaglandin F1 alpha increased significantly when sucralfate was given. Sucralfate did not affect serum ethanol levels, nor did ethanol affect prostanoid synthesis. It is concluded that sucralfate provides significant protection to the human gastric mucosa against ethanol injury, and that this may be partly due to increased prostanoid synthesis.
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PMID:Sucralfate protection of human gastric mucosa against acute ethanol injury. 264 75

Sucralfate promotes the healing of peptic ulcers and, in large doses, increases gastric mucosal prostaglandins. The present study was designed to further elucidate the protective effect of sucralfate and to evaluate the role of prostaglandins in this action. Eight chair-adapted rhesus monkeys received a subcutaneous injection of either 150 mg/kg of aspirin or vehicle in combination with either a therapeutic oral dose of sucralfate (50 mg/kg X day) or water. Gastric soluble mucus concentration was determined in samples of gastric juice by Alcian blue dye binding of acidic glycoproteins, and mucus output was determined using a technetium 99m-diethylenetriaminepentaacetic acid dilution technique. Monkeys underwent endoscopy to assess gastric mucosal damage, which was ranked blindly on a scale of 0-5, and to obtain biopsy specimens for determination of mucosal prostaglandin E2, prostaglandin F2 alpha, and 6-keto-prostaglandin F1 alpha. Aspirin did not alter soluble mucus but did significantly increase gastric mucosal damage and suppress tissue levels of all prostaglandins. Sucralfate significantly increased the output of soluble mucus, even after aspirin treatment, and protected against aspirin-induced damage, although it did not modify aspirin-induced suppression of prostaglandins. These results suggest that the gastric protection afforded by sucralfate is related to a prostaglandin-independent increase in mucus production.
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PMID:Gastric protection by sucralfate. Role of mucus and prostaglandins. 346 Sep 26