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)

Sucralfate protects the stomach against a number of experimental damaging agents and is efficacious in the treatment of peptic ulcer disease. It binds with acidity to the base of an ulcer to form a protective barrier. Sucralfate also enhances prostaglandin synthesis and release in the mucosa. In this study, the rat stomach was examined to determine sucralfate's interaction with gastric mucus. Mucus in the rat stomach forms a distinct and continuous blanket. In snap-frozen samples, pretreatment with phosphate-buffered saline as a control shows a layer of mucus of homogeneous structure thinner than the homogeneous layer after pretreatment with antibodies developed against rat gastric mucus. Pretreatment with the surface protective agent sucralfate shows some increase in the thickness of mucus with a thin dense sublayer adjacent to the epithelium and a less dense-appearing outer zone of variable thickness. Analysis of x-rays generated by the electron beam on windows of mucus and epithelium showed the expected gradients of sodium, potassium, chloride, and sulfur. The percentage of aluminum and sulfur in the mucus was higher in sucralfate-treated samples than in controls. Interaction between sucralfate and gastric mucus needs further investigation.
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PMID:Sucralfate interactions with gastric mucus. 273 36

Sucralfate was tested in a rabbit model for its ability to prevent experimental esophagitis. Esophagitis was assessed by gross appearance and microscopic examination by an uninformed observer. In addition, the permeability of the esophagus to a number of probe molecules was measured to assess barrier function. Animals were exposed for 1 h to either acid alone (HCl at pH 2), acid plus pepsin (0.8 mg/ml), or acid plus taurocholic acid (5 mM), as well as to the same injurious agents with the addition of 1 g of sucralfate. At the completion of this hour, the perfusate was removed and all animals were again perfused for 1 h with HCl at pH 2 while mucosal permeability was assessed by measuring erythritol, glucose, potassium, and sodium fluxes. The animals were then killed. Sucralfate significantly diminished esophagitis and the attendant mucosal permeability changes induced by pepsin. The viscous sucralfate gel was shown to adhere tenaciously to the esophageal mucosa, but this characteristic of sucralfate was found not to be critical for its protective action because a clear sucrose sulfate solution with no gel present was also protective. Hence, it was not necessary for the gel to be present for the drug to be effective. Several in vitro tests suggested that the clear sucrose sulfate solution, like the sucralfate gel, probably acts through a topical protectant effect, rather than through pepsin inactivation. Although the degree of esophagitis induced by the bile acid was significantly less than that observed with pepsin, the mucosal permeability changes were comparable. Sucralfate did not significantly reduce the flux rates of glucose, potassium, and sodium nor did it affect the morphology of the mucosa after exposure to taurocholic acid. In conclusion, the binding of sucralfate to pepsin substrates in tissue results in this agent being very effective in preventing experimental peptic esophagitis.
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PMID:Sucralfate prevents experimental peptic esophagitis in rabbits. 391 56

14C-Sucralfate, a basic aluminum salt of 14C-sucrose sulfate, or potassium 14C-sucrose sulfate was administered orally to rats with acetic acid-induced gastric ulcer. The radioactivities representing specific binding of the sucrose sulfate moiety were found significantly higher in ulcer sections of the stomach, with the mean within-animal ulcer/non-ulcer ratio attaining 6, 7, 12 and 2.5, respectively, at 1, 3, 6 and 24 h after 14C-sucralfate administration. Microautoradiography provided direct in vivo evidence for binding of the 14C-sucrose sulfate moiety to exuded proteins resulting in effect in formation of a pepsin-resistant barrier over the surface of an ulcer crater. No comparable findings were obtained in the area of normal mucosa. The administration of 14C-sucralfate was associated with much greater and longer-sustained binding to the ulcer lesion and retention in the stomach and duodenum than simple administration of the soluble potassium salt. These findings not only demonstrate therapeutically significant effects of basic aluminum compoundation but also substantiate likely differences from pepsin inhibitors such as amylopectin sulfate in terms of presence or absence of adhesiveness, local barrier effects, and long duration of actions.
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PMID:Selective binding of sucralfate to ulcer lesion. II. Experiments in rats with gastric ulcer receiving 14C-sucralfate or potassium 14C-sucrose sulfate. 689 77

We have established models of cell damage induced by acid and pepsin using rat gastric epithelial cells (RGM1). In the present study, the effects of aluminum hydroxide [Al(OH)3] and potassium sucrose octasulfate (KSOS), which are components of sucralfate, and sucralfate on cell damage and peptic activity of pepsin were examined. Pretreatment of cells with sucralfate (0.1-3 mg/ml) or Al(OH)3 (0.1-1 mg/ml) for 2 hr prevented both acid- (pH 4.0) and pepsin- (pH 4.5) induced cell damage. However, KSOS (0.1-1 mg/ml) did not show any effects on two different types of cell damage. The peptic activity of pepsin at pH 4.5 was about 10% of that at pH 2.0. Sucralfate and KSOS slightly inhibited peptic activity at pH 4.5. Al(OH)3 inhibited peptic activity by approximately 50%; however, no concentration-dependent pattern was observed. Pepstatin (0.003-0.1 mg/ml), a specific inhibitor of pepsin, inhibited the peptic activity in a concentration-dependent manner. Here, we confirmed that sucralfate and Al(OH)3 have cytoprotective effects against acid- and pepsin-induced cell damage. The mechanism behind the cytoprotective effects of sucralfate seems to relate to adhesion of the cell surface and neutralization of hydrogen ion by aluminum that prevents the penetration of hydrogen ions into the cells.
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PMID:Effects of sucralfate and its components on acid- and pepsin-induced damage to rat gastric epithelial cells. 933 82