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

The mucous gel maintains a neutral microclimate at the epithelial cell surface, which may play a role in both the prevention of gastroduodenal injury and the provision of an environment essential for epithelial restitution and regeneration after injury. Enhancement of the components of the mucous barrier by sucralfate may explain its therapeutic efficacy for upper gastrointestinal tract protection, repair, and healing. We studied the effect of sucralfate and its major soluble component, sucrose octasulfate (SOS), on the synthesis and release of gastric mucin and surface active phospholipid, utilizing an isolated canine gastric mucous cells in culture. We correlated these results with the effect of the agents on mucin synthesis and secretion utilizing explants of canine fundus in vitro. Sucralfate and SOS significantly stimulated phospholipid secretion by isolated canine mucous cells in culture (123% and 112% of control, respectively). Indomethacin pretreatment significantly inhibited the effect of sucralfate, but not SOS, on the stimulation of phospholipid release. Administration of either sucralfate or SOS to the isolated canine mucous cells had no effect upon mucin synthesis or secretion using a sensitive immunoassay. Sucralfate and SOS did not stimulate mucin release in the canine explants; sucralfate significantly stimulated the synthesis of mucin, but only to 108% of that observed in untreated explants. No increase in PGE2 release was observed after sucralfate or SOS exposure to the isolated canine mucous cells. Our results suggest sucralfate affects the mucous barrier largely in a qualitative manner. No increase in mucin secretion or major effect on synthesis was noted, although a significant increase in surface active phospholipid release was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of sucralfate on components of mucosal barrier produced by cultured canine epithelial cells in vitro. 147 34

We studied whether sucralfate's protection of the gastric mucosa against ethanol induced injury in the rat is prostaglandin mediated. Rats received intragastric pretreatment: i) saline, ii) sucralfate, and iii) indomethacin-sucralfate. One hour later gastric contents were obtained for measurements of prostaglandin E2 and 2 ml of 100% ethanol were instilled. Rats were sacrificed 1 h later. The gastric mucosa was assessed: a) macroscopically by planimetry, b) by quantitative histology, and c) by measurements of gastric volume, pH and sodium. We found that sucralfate significantly increased gastric luminal release of prostaglandin E2. The increase was completely abolished by indomethacin pretreatment. Sucralfate protected the gastric mucosa against ethanol injury reducing macroscopic and histologic necrosis. Indomethacin (prostaglandin synthetase inhibitor) given 2 h prior to sucralfate markedly abolished its protective action against ethanol induced necrosis by 70%. These findings indicate that prostaglandins mediate some of the protective action of sucralfate. Sucralfate appears to have additional protective action which is prostaglandin independent.
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PMID:Sucralfate protection of the gastric mucosa against ethanol-induced injury: a prostaglandin-mediated process? 659 42

Nicotinamide, a precursor of nicotinamide adenine dinucleotide (NAD(+)), is an essential nutrient for cell growth that participates in DNA repair and energy production. Nonsteroidal anti-inflammatory drugs (NSAIDs)-induced gastropathy is an intricate process involving gastric mucus depletion, increased microvascular permeability, nitric oxide imbalance, as well as free radical production. The present study was conducted to test for the possible gastroprotective effect of nicotinamide utilizing an acute indomethacin-induced gastric ulcer model. Sucralfate possesses antiulcer/antioxidant properties; hence it was used as the reference drug. Indomethacin resulted in hemorrhagic mucosal lesions, increased microvascular permeability, and reduced the gastric mucosal contents of nitric oxide and mucus. Moreover, it produced an imbalance in the mucosal redox state as indicated by a decline of glutathione and glutathione peroxidase, which were associated with increased lipid peroxides. Comparable to sucralfate, nicotinamide markedly decreased the severity of indomethacin-induced gastric lesions and restored the levels of altered biochemical parameters. Gastroprotection afforded by nicotinamide is possibly mediated by conservation of gastric mucus, as well as nitric oxide contents, enhanced gastric microvascular permeability, and its antioxidant properties.
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PMID:Nicotinamide alleviates indomethacin-induced gastric ulcers: a novel antiulcer agent. 1985 87