Metabolic Fate of a New Anti-ulcer Drug (+)-(1R,4aS,10aR)-1,2,3,4,4a,9,10,10a-Octahydro-1,4a-dimethyl-7-(1-methylethyl)-6-sulfo-1-phenanthrenecarboxylic Acid 6-Sodium Salt Pentahydrate (TA-2711). II. Distribution in the Rat Stomach.

Ito, Yutaka; Sugawara, Yoichi; Takaiti, Osasi; Nakamura, Susumu

doi:10.1248/bpb1978.14.547

Cited by 30 publications

(22 citation statements)

References 6 publications

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“…e In rats in the ecabet sodium group (group C) in which esophagitis did not develop, the findings were nearly the same as those in the control animals, while in those in which esophagitis developed, the histopathological changes were milder than those in group B (H&E, ϫ 16) a d e b c aggravation, as it selectively covers the damaged region of the digestive tract. 8 Based on the same mechanism of action, a covering effect on an inflammatory region, this drug could be expected to have a therapeutic effect in reflux esophagitis. However, as appropriate chronic experimental models for acid reflux have not been established, drugs used for the treatment of reflux esophagitis have been evaluated for efficacy in rat models of acute reflux esophagitis.…”

Section: Discussionmentioning

confidence: 99%

Effects of ecabet sodium on experimentally induced reflux esophagitis

Omura

Kashiwagi

Chen

et al. 2000

Journal of Gastroenterology

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We investigated the effects of ecabet sodium on experimentally induced reflux esophagitis in rats. Three groups of rats, i.e., a control group, esophagitis group, and an ecabet sodium group (25mg/kg given twice daily) were used. The number of animals which developed esophagitis, the extent of the lesions, and the esophagitis lesion index were assessed 3 weeks after the start of the experiment, and the lesions were evaluated histopathologically. All nine surviving rats in the esophagitis group developed esophagitis, and the esophagitis lesion index was 32.6 +/- 7.2 (mean +/- SE) per animal. Histopathologically, thickening of the epithelium, elongation of papillae of the lamina propria into the epithelium, and infiltration of the lamina propria by lymphocytes, eosinophils, plasmacytes, and neutrophils, were observed. Interruption of the lamina of the muscularis mucosae was also observed, and there was marked proliferation of collagen fibers in the submucosa and lamina propria. In the ecabet sodium group, esophagitis developed in five of the nine surviving animals (55.6%), but the esophagitis lesion index was 1.89 +/- 0.73 per animal, which was significantly lower than that in the esophagitis group. The histopathological changes in the rats which developed esophagitis were milder in the ecabet sodium group than in the esophagitis group. These results suggest that ecabet sodium could be useful for the prevention of reflux esophagitis.

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Section: Discussionmentioning

confidence: 99%

Effects of ecabet sodium on experimentally induced reflux esophagitis

Omura

Kashiwagi

Chen

et al. 2000

Journal of Gastroenterology

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“…Ecabet is a locally acting agent with low absorption, showing a high affinity for the gastric mucus (1,2). Mechanisms of action have been reported as follows: it enhances gastric epithelial restitution, facilitates mucus synthesis and secretion, increases gastric mucosal blood flow and bicarbonate secretion, enhances gastric mucosal prostaglandin E 2 production, and inhibits gastric pepsin and pepsinogen activity (3)(4)(5).…”

mentioning

confidence: 99%

Therapeutic Effects of Ecabet Sodium, an Antiulcer Drug, on Dextran Sodium Sulfate–Induced Ulcerative Colitis in Rats

Noto

Yamada²,

Inui³

et al. 2005

Dig Dis Sci

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Ecabet, an antiulcer drug, is reported to be effective in patients with ulcerative colitis. We investigated the effect of ecabet enema on ulcerative colitis in rats and some mechanisms underlying this effect. In vivo ecabet enema showed a therapeutic effect in the rat ulcerative colitis model induced by dextran sodium sulfate in the drinking water. The amount of ecabet bound to damaged mucosa was higher than that bound to normal mucosa 30 min after intrarectal administration. In vitro ecabet accelerated the restitution of epithelial cells, which was not affected by a TGF-beta antibody. Ecabet inhibited the leukotriene B4 production and 5-lipoxygenase activity in human neutrophils. In conclusion, ecabet enema showed a therapeutic effect in rats with ulcerative colitis. This effect may be attributable to the high binding affinity for damaged mucosa, the acceleration of restitution, and the inhibition of leukotriene B4 production.

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“…Ecabet sodium is distributed mainly in the gastrointestinal tract, and the intestinal absorption rate is estimated to be only 3.4 to 7.0% of the dose administered in rats (11). Furthermore, the high affinity of ecabet sodium for the stomach wall (12) seems to contribute to its antiulcer effect. In regard to H. pylori, we have found that ecabet sodium inhibits the urease activity of a crude enzyme preparation from H. pylori in a time-and concentration-dependent manner at acidic pH (15).…”

mentioning

confidence: 99%

Bacterial activity of a new antiulcer agent, ecabet sodium, against Helicobacter pylori under acidic conditions

Shibata

Ito

Hongo

et al. 1995

Antimicrob Agents Chemother

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Helicobacter pylori NCTC 11637, which is nonviable at pH 3.0, became viable after addition of 10 mM urea owing to ammonia production by urease. In a buffer supplemented with urea, ecabet sodium decreased both the production of ammonia and the number of viable cells of H. pylori NCTC 11637 and changed the bacteria from the bacilliform to the horseshoe or doughnut shape in a concentration-dependent manner. In particular, ecabet sodium (2 and 4 mg/ml) decreased the number of viable cells below the control level. Benzohydroxamic acid, a urease inhibitor, also caused a decrease in ammonia production accompanied by a decrease in the number of viable cells and changed the morphological form at pH 3.0, but the number of viable cells was not lowered below the control level. In buffers at various pHs without urea, ecabet sodium showed a concentrationdependent bactericidal effect on H. pylori at pHs 4.0 and 5.0 but not at pHs 6.0 and 7.0 while benzohydroxamic acid caused only a slight decrease in the number of viable cells at pH 4.0. These results suggest that ecabet sodium has strong bactericidal activity in addition to its urease-inhibiting activity under acidic conditions.

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Metabolic Fate of a New Anti-ulcer Drug (+)-(1R,4aS,10aR)-1,2,3,4,4a,9,10,10a-Octahydro-1,4a-dimethyl-7-(1-methylethyl)-6-sulfo-1-phenanthrenecarboxylic Acid 6-Sodium Salt Pentahydrate (TA-2711). II. Distribution in the Rat Stomach.

Cited by 30 publications

References 6 publications

Effects of ecabet sodium on experimentally induced reflux esophagitis

Effects of ecabet sodium on experimentally induced reflux esophagitis

Therapeutic Effects of Ecabet Sodium, an Antiulcer Drug, on Dextran Sodium Sulfate–Induced Ulcerative Colitis in Rats

Bacterial activity of a new antiulcer agent, ecabet sodium, against Helicobacter pylori under acidic conditions

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