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)

We have studied the effect of the aluminum complex of sucrose sulphate (Sucralfate suspension) and the sodium salt of sucrose sulphate (sodium sucrose sulphate solution) on patients with keratoconjunctivitis sicca. Eyes treated with either of these two drugs showed a decrease in painfulness and blurring of vision. On examination the surface area of the corneal lesions, stained with fluorescein, diminished during treatment. As for the difference in effect between the two eyedrops, the solution was better tolerated.
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PMID:Sucralfate and sodium sucrose sulphate in the treatment of superficial corneal disease in keratoconjunctivitis sicca. 141 98

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

Studies using a gastric chamber model demonstrated that sucralfate protected the rat gastric mucosa against hemorrhagic erosions induced by 40 percent ethanol and by acidified 80 mM sodium taurocholate. Protection required continuous contact of sucralfate with the gastric mucosa but it occurred without the production, by sucralfate alone, of significant damage to the luminal epithelium. Ultrastructural examination indicated that sucralfate stimulated mucus secretion by surface epithelial cells. Furthermore, sucralfate was "cytoprotective" in that, in addition to its anti-ulcer effects, it significantly reduced the damaging effects of luminal ethanol on the surface epithelium. Luminal stasis also significantly reduced the extent of hemorrhagic erosions produced by both ethanol and sodium taurocholate, but the most effective reduction in erosions occurred when sucralfate and luminal stasis were combined. Pretreatment with indomethacin abolished the protection provided by luminal stasis, but this protection was restored by sucralfate. Thus, these studies suggest that protection of the gastric mucosa by sucralfate results in part from effects on the unstirred layer. Sucralfate or its products also interact with the epithelial cells and stimulate mucus release and synthesis or release of inflammatory mediators.
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PMID:Protection of rat gastric mucosa by sucralfate. Effects of luminal stasis and of inhibition of prostaglandins synthesis. 273 27

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

The effect of Campylobacter pylori infection and sucralfate treatment on the ion-exchange property of human gastric mucus from 17 human postmortem stomachs was investigated in an in vitro chamber. Of the 10 stomachs not infected with C. pylori mucus from 4 stomachs had a 'normal' Na+/H+ exchange capacity, whereas 6 were without a Na+/H+ exchange capacity. The Na+/H+ exchange capacity of the seven stomachs infected with C. pylori was half that of the four 'normal' uninfected stomachs. Sucralfate significantly improved the Na+/H+ exchange capacity of mucus from C. pylori-infected stomachs and from the uninfected stomachs without Na+/H+ exchange. This study shows that impairment of the Na+/H+ exchange capacity of gastric mucus is associated with C. pylori infection and that sucralfate improves the Na+/H+ exchange capacity of gastric mucus.
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PMID:Na+/H+ ion-exchange property of postmortem human gastric mucus. The effects of Campylobacter pylori infection and sucralfate. 279 81

Misoprostol, a PGE1 derivative that inhibits gastric acid secretion in rats, was compared with cimetidine and sucralfate in several rat experimental ulcer models. Gastric lesions were produced by aspirin, indomethacin, stress, sodium taurocholate, and ethanol. In all tests, misoprostol (50, 100, and 200 micrograms/kg) and cimetidine and sucralfate (50, 100, and 200 mg/kg) were administered intragastrically. Misoprostol protected against gastric lesions in all five experimental ulcer models at lower than gastric antisecretory doses. Cimetidine protected in the indomethacin, aspirin, and stress models, but only at gastric antisecretory doses, and did not protect against lesion formation in the ethanol and taurocholate models. Sucralfate, over the dose range tested, was not consistently protective in any of the five experimental ulcer models. It is concluded that misoprostol provides gastric mucosal protection against a wide variety of noxious agents by means of a unique mechanism and that reduction of gastric acid secretion is not required, as it is with cimetidine, for the protective effect.
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PMID:Comparative mucosal protective properties of misoprostol, cimetidine, and sucralfate. 308 Feb 94

The protective effect of sucralfate against gastric and intestinal mucosal damage was studied in rats. Sucralfate (125 mg) significantly reduced gastric mucosal lesion formation induced by s.c. administration of indomethacin (30 mg/kg) or intragastric administration of aspirin (100 mg/kg), HCl (0.6 N), NaOH (0.2 N) or sodium taurocholate (30 mM). Furthermore, when given in three doses of 125 mg each, sucralfate significantly decreased the development of small intestinal lesions induced by indomethacin in the re-fed rat. Gastric mucosal cyclooxygenase activity in sucralfate-treated rats expressed as prostaglandin E2 formation--388 +/- 140 (ng/g wet weight; mean +/- SE)--was significantly higher (P less than 0.01) than its activity in the control--264 +/- 62 (ng/g wet weight). Sucralfate also slightly, but significantly, decreased indomethacin-induced gastric mucosal cyclooxygenase inhibition. Intestinal mucosal cyclooxygenase activity was not affected by sucralfate. The results suggest that gastric and intestinal mucosal damage induced by various ulcerogens is significantly reduced by sucralfate. Sucralfate-induced stimulation of endogenous gastric mucosal prostanoid formation may in part explain its effective protective properties.
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PMID:Sucralfate protection against gastrointestinal damage: possible role of prostanoids. 309

Rats pretreated with dilute ethanol, dilute hydrochloric acid, or dilute sodium hydroxide had significantly less gastric mucosal damage when they were exposed 15 or 30 minutes later to strong irritants. The dilute agents, known as mild irritants, also caused an increase in the production of gastric mucosal prostaglandin E2 at the 15- and 30-minute dosing intervals. This suggests that the mild irritants are only effective in providing gastric mucosal protection when they increase gastric production of prostaglandin E2. Sucralfate treatment also caused an increase in gastric mucosal production of prostaglandin E2 at only the 15- and 30-minute dosing intervals. In contrast, pretreatment with sucralfate protected against the damaging effects of the strong irritants for at least 480 minutes. Therefore, prostaglandin E2 may play a role in sucralfate's protective effect at short dosing intervals, but at longer intervals, when prostaglandin E2 changes were not observed, sucralfate was still found to be very effective in reducing the severity of gastritis. This suggests that sucralfate acts, at least in part, through some other mechanism(s) besides increasing gastric mucosal prostaglandin E2 production.
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PMID:Effects of sucralfate or mild irritants on experimental gastritis and prostaglandin production. 347 60

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

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


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