16-16-dimethylprostaglandin-e2 and bismuth-tripotassium-dicitrate

16-16-dimethylprostaglandin-e2 has been researched along with bismuth-tripotassium-dicitrate* in 3 studies

Other Studies

3 other study(ies) available for 16-16-dimethylprostaglandin-e2 and bismuth-tripotassium-dicitrate

ArticleYear
Epidermal growth factor (EGF) in the gastroprotective and ulcer healing actions of colloidal bismuth subcitrate (De-Nol) in rats.
    Gut, 1988, Volume: 29, Issue:7

    Colloidal bismuth subcitrate (CBS; De-Nol) exhibits gastroprotective properties in experimental animals and enhances the healing of chronic gastroduodenal ulcers, but the mechanisms of these actions have not been entirely elucidated. The present study was designed to determine whether epidermal growth factor (EGF), which also has gastroprotective and ulcer healing properties, contributes to the action of De-Nol on the stomach in rats. It was found that De-Nol protects the gastric mucosa against ethanol damage and that this is accompanied by increased mucosal generation of prostaglandins (PG). Removal of the endogenous source of EGF (sialoadenectomy) did not significantly decrease the protective and PG stimulating effects of De-Nol. Pretreatment with exogenous EGF partially protected the stomach against ethanol injury, but did not influence the protective action of De-Nol in sialoadenectomised animals. De-Nol, like EGF given orally, enhanced the healing of chronic gastric and duodenal ulcers induced by serosal acetic acid. De-Nol was found to bind EGF in a pH-dependent manner and to accumulate it in ulcer area. Thus the peptide is available locally in high concentrations to accelerate the re-epithelialisation and tissue repair of the ulcerated mucosa. These ulcer healing effects of De-Nol were reduced by sialoadenectomy and restored in part by oral administration of EGF. We conclude that salivary glands in rats are not essential for the gastroprotection induced by De-Nol, but seem to play an important role in the ulcer healing action of this drug possibly via an EGF mediated mechanism.

    Topics: 16,16-Dimethylprostaglandin E2; Animals; Anti-Ulcer Agents; Bismuth; Epidermal Growth Factor; ErbB Receptors; Gastric Mucosa; Male; Organometallic Compounds; Peptic Ulcer; Rats; Rats, Inbred Strains; Submandibular Gland

1988
Studies on the gastroprotective and ulcer-healing effects of colloidal bismuth subcitrate.
    Digestion, 1987, Volume: 37 Suppl 2

    We investigated the gastroprotective effects of colloidal bismuth subcitrate (CBS, De-Nol) in comparison with agents such as sucralfate and methylated PGE2. Both CBS and sucralfate given orally prevented dose dependently the formation of gastric lesions by acidified aspirin, ethanol and restraint stress, CBS being more potent on a weight-to-weight basis than sucralfate. CBS and sucralfate were also equally effective in enhancing the healing rate of chronic gastric and duodenal ulcer induced by serosal application of acetic acid, while methylated PGE2 was completely ineffective in this model. Non-colloidal bismuth subnitrate, in contrast to CBS, was ineffective against stress-induced lesions. CBS stimulated mucosal generation and luminal release of PGE2 dose dependently.

    Topics: 16,16-Dimethylprostaglandin E2; Animals; Anti-Ulcer Agents; Aspirin; Immersion; Organometallic Compounds; Rats; Rats, Inbred Strains; Stomach Ulcer; Stress, Physiological; Sucralfate

1987
Advances in the understanding of the mechanism of cytoprotective action by colloidal bismuth subcitrate.
    Scandinavian journal of gastroenterology. Supplement, 1986, Volume: 122

    This study was designed to compare the gastroprotective effects of colloidal bismuth subcitrate (CBS) with those of sucralfate and methylated analog of prostaglandin E2 (PGE2) against acute gastric lesions induced by absolute ethanol, acidified aspirin (ASA), and water immersion and restraint stress in rats. When given orally, both CBS and sucralfate prevented in a dose-dependent way the formation of gastric lesions induced by all three ulcerogens, CBS being about 7, 2, and 20 times more potent, respectively on a weight-to-weight basis than sucralfate. Methylated PGE2 was also highly effective against these ulcerogens. Bismuth subnitrate was ineffective against acute gastric lesions induced by stress conditions. The protection of both CBS and sucralfate was reversible when the animals were pretreated with indomethacin to suppress the generation of endogenous prostaglandins. Since CBS and sucralfate increased the production of PGE2 in the gastric mucosa, we postulate that their gastric protective action may be mediated, at least partly, by mucosal prostaglandins.

    Topics: 16,16-Dimethylprostaglandin E2; Animals; Bismuth; Dinoprostone; Gastric Mucosa; Organometallic Compounds; Prostaglandins E; Rats; Rats, Inbred Strains; Stomach Ulcer; Sucralfate

1986