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)

Stress ulcer was studied from the view point of cytokinetics by applying 3H-TdR double pulse labelling technique. In combination with clinical practice, the effects of three common preventive drugs Sucralfate (SCR), 25% glucose and Danshen compound were investigated. The results indicated that when stress ulcer developed, the Ts and Tc stage of gastric mucosa in the rat was much prolonged (P less than 0.01), an apparent lowering of 3H-TdR labelling index appeared (P less than 0.01), and significant impact of cytokinetic changes of mucosal cell was only seen in the region of the gastric body but not at the antral portion. SCR, 25% glucose and compound Danshen displayed a considerable protective action against ulceration and this could facilitate the recovery of Ts, Tc stage to normal range (P less than 0.01).
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PMID:[Experimental cytokinetic study of gastric mucosa in stress ulcer]. 166 77

Sucralfate, an aluminum salt of sucrose octasulfate, has been shown to be effective in reducing the discomfort of radiation therapy-induced oral mucositis. This study was done to determine whether sucralfate could be used as a nutritional source for dental caries-producing organisms. Three Streptococcus strains were cultured in a defined medium. Sucralfate powder was evaluated for its ability to be used as a carbohydrate food source by these organisms. The addition of sucralfate alone did not stimulate the organism's growth. The addition of sucralfate and glucose resulted in less growth than the addition of glucose alone. Increasing the sucralfate concentration from 1% to 10% in the glucose-containing cultures resulted in statistically significant growth inhibition (p less than 0.02). Sucralfate appears to have no cariogenic potential and may have some cariostatic potential.
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PMID:The effect of sucralfate on the growth of cariogenic streptococci. 177 88

The first part of the study consisted of 110 rats in 11 groups with ten rats in each. Nine of the groups were fed nutrient solutions of different compositions, antacid and sucralfate through orogastric tube during induction of stress ulcer by restraint and a cold ambient temperature. One group served as a control group and received no feeding and the 11th group was given cimetidine intraperitoneally. The extensiveness of the stress effect was estimated in each group by the number of rats with ulcer as percentage, the mean number of ulcers in each rat, the mean distribution of ulcers of different sizes, the mean total of mucosal damage in each rat and the contribution of ulcers of a different size to the total mucosal damage. The results showed that cimetidine is an effective protector against stress ulcer. Guar gum, Intralipid (fat emulsion), egg protein and 30 per cent glucose are slightly weaker protectors than cimetidine but much stronger than 10 per cent glucose wheat flour and distilled water. Sucralfate increased the susceptibility to stress ulcer. The second part of the study consisted of 86 rats. It showed, that guar gum increased the healing rate of stress ulcers. During a 30 hour treatment period after four hours of stress, the rats fed guar gum (n = 30) showed a lower (p less than 0.001) number of ulcers than the control rats fed normal rat food (n = 26) or immediately after the four hours of stress (n = 30). The mechanisms suggested for ulcer prevention and increased ulcer healing rate found herein may be due to reduced acidity, increased local mucosal supply of energy and mechanical protection.
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PMID:The protective effect of nutrients against stress induced gastric ulcers in the rat. 282 67

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