Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of zinc sulphate pretreatment on the formation of gastric ulcers, changes in intragastric pressure and changes in the gastric mucosal mast cell count induced by electrical vagal stimulation were studied in anaesthetized rats. Vagal stimulation produced a high gastric glandular ulcer incidence and ulcer index, increased the intragastric pressure, and reduced the number of granulated mast cells in the gastric mucosa and submucosa. Pretreatment with zinc sulphate (22, 44 ot 88 mg/kg), injected i.p. 48 h beforehand, reversed the changes in these parameters in a dose-related manner. These observations suggest that the inhibitory effects of zinc sulphate on mucosal mast cell degranulation may account for its ability to antagonise vagal-induced gastric glandular ulceration. The mechanisms involved in the aetiology of this type of gastric ulcer are discussed in the light of these results.
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PMID:The effects of zinc sulphate on vagal-induced mast cell changes and ulcers in the rat stomach. 88 Sep 79

A small ulcer produced in vitro by monopolar electrocoagulation on endoscopically obtained human antral biopsies and incubated in Trowel T-8 medium at 37 degrees C for 8 h has many histologic features of chronic gastric ulcer in man. Zinc sulfate and acetylcysteine in low concentrations had a significant healing effect in this ulcer model. Since the beneficial effect of zinc sulfate and acetylcysteine was counteracted by N-ethylmaleimide, a known blocker of sulfhydryl compounds, the beneficial effect of these two compounds probably was mediated through sulfhydryl compounds. Using special stain, N-(4-aminophenyl)maleimide, the sulfhydryl groups were localized in the epithelial cells of the surface layer and gastric glands.
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PMID:Effect of zinc sulfate and acetylcysteine on experimental gastric ulcer: in vitro study. 128 68

A slow-release zinc complex, zinc monoglycerolate (ZMG) was examined for its potential gastroprotective activity in various gastric ulcer models. These models comprised (a) oral or parenteral non-steroidal anti-inflammatory drugs (NSAIDs) given to rats whose gastrointestinal mucosa was pre-sensitized by prior development of arthritis, oleyl alcohol-induced inflammation and cold exposure, (b) oral ethanol (12.5-100%) with and without added 4% HCl, (c) intraperitoneal reserpine (5 mg kg-1) in arthritic and normal rats and in normal mice, (d) oral NSAIDs given to mice in which acid and pepsin production was stimulated by co-administration of intraperitoneal bethanechol chloride (5 mg kg-1) to enhance ulcer development, and (e) NSAIDs given to carrageenan-inflamed rats to determine effects of ZMG on paw inflammation. In these models, ZMG given orally was effective in preventing development of gastric lesions, except with propionic acid NSAIDs; the effective doses being apparently dependent on the severity of the mucosal injury. In many of the models ZMG was superior to zinc sulphate and other zinc salts or metal ion complexes investigated but was slightly more effective or equipotent compared with zinc acexamate. ZMG did not impair the anti-oedemic effects of NSAIDs. ZMG is thus an effective agent in preventing ulcer development in a wide range of model systems and may be more effective than zinc salts because of the controlled slow-release of zinc from the complex.
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PMID:Anti-ulcer activity of a slow-release zinc complex, zinc monoglycerolate (Glyzinc). 135 71

The effects of zinc sulphate on gastric ulcer healing rate and mucosal mucus content of acetic acid-induced ulceration in rats have been assessed. Daily treatment with zinc sulphate progressively accelerated ulcer healing in a dose-dependent manner with a significant increase observed on day 15 after ulcer induction in rats treated with 44 and 88 mg kg-1 zinc sulphate. A significant increase in gastric mucosal adherent mucus was also observed in those animals treated with 88 mg kg-1 zinc sulphate. The results suggest that a minimum treatment period of 15 days is needed for the zinc sulphate to be effective, and that zinc ions may promote gastric ulcer healing by enhancing mucus formation to prevent acid back-diffusion into the gastric mucosa.
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PMID:Effect of zinc sulphate on acetic acid-induced gastric ulceration in rats. 198 7

Zinc sulfadiazine (ZnSD) 50, 100, 200 mg/kg ig inhibited the formation of gastric ulcer induced by indomethacin, stress and pyloric ligation in rats respectively and showed dose-dependently. ZnSD 200 mg/kg ig accelerated the healing of gastric ulcer induced by acetic acid. ZnSD 25 mg/kg ig was effective in preventing ethanol-induced damage of rat gastric mucosa. The amount of gastric mucus glycoprotein in gastric tissues was increased by ZnSD. In general, ZnSD did not influence the volume of gastric juice and pepsin output, but ZnSD 200 mg/kg ig decreased gastric acidity. In vitro, ZnSD also influenced the neutralization of acid. It is suggested that antiulcer action of ZnSD may be related to its preservation of the gastric mucosal barrier and neutralization of acid.
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PMID:[Anti-gastric ulcer activity of zinc sulfadiazine in rats]. 213 Jun 5

We have tested the ability of zinc acexamate (ZAC) to prevent platelet-activating-factor (Paf) induced gastric damage in rats. Lesions were characterized by a vascular congestion affecting the entire mucosa, oedema, haemorrhage and frequent necrosis of the more superficial areas. The gastric damage appearing after Paf was accompanied by degranulation of gastric mast cells. Leukocytes were often seen at the submucosal level. Oral pretreatment with ZAC reduced in a dose-dependent manner both gastric damage and mast cell degranulation observed after Paf. ZAC administered orally at a dose of 100 mg kg-1 statistically inhibited (p less than 0.01) gastric damage and mast cell degranulation. ZAC did not affect the hypotension induced by Paf confirming that gastric damage and hypotension appearing in rats after Paf administration are two independent phenomena. The present findings indicate that the inhibitory effect of ZAC upon gastric lesions induced by Paf may be related to the different protective actions exhibited by this zinc compound in a wide variety of experimental models of gastric ulcer.
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PMID:Zinc acexamate reduces gastric damage induced by platelet-activating factor. 260 1

Effects of zinc in gastric ulcer have been reviewed through investigations carried out on zinc acexamate (ZAC). ZAC is an organic compound that has been shown to possess an experimental antiulcer effect and a wide therapeutic index, making it a useful drug in the treatment of peptic ulcer disease. ZAC protects from ulceration in several experimental models such as pylorus occlusion, reserpine-induced ulcer, necrotizing agents, PAF-induced ulcer and cold-restraint stress. ZAC first reduces the gastric acid output by inhibiting the mast cell degranulation, an action likely to be mediated through a membrane stabilizing action. Secondly, it enhances the mucosal protection factors by increasing mucus secretion, inhibiting the H+ retrodiffusion and improving microcirculation. ZAC is also effective in acetic acid-induced chronic ulcer, restoring the continuity of the damaged mucosa. Several clinical trials have shown the usefulness of ZAC in acute and maintenance treatment of both gastric and duodenal ulcers. Endoscopic studies showed that ZAC reduced the inflammatory processes (gastritis and duodenitis) associated with ulcer healing. This reduction was statistically significant and not observed with other comparative treatments (H2-antagonists). The observed side-effects were minimal and affected less than 2% of treated patients. The pharmacological profile, clinical effectiveness and good tolerance of ZAC suggest this compound as an interesting option in the treatment of peptic disease.
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PMID:Zinc compounds, a new treatment in peptic ulcer. 266 Nov 83

The aetiology of ethanol-induced gastric ulceration, and its interaction with zinc, were studied in rats. Oral administration of ethanol (40, 50 or 80%) to conscious rats reduced the stomach mucus content and increased gastric ulcer formation in a concentration-dependent manner. Histological examination indicated that mucus, both on the surface and within the epithelium, was depleted because of epithelium being shed from the gastric mucosa. Zinc sulphate abolished mucus loss and ulcer formation in the ethanol-treated animals. Using an ex-vivo gastric chamber preparation in anaesthetised animals, it was found that an ethanol (50%)-HCl (100 mmol/l) solution produced severe glandular haemorrhagic ulceration, elevated Na+, K+ and protein levels in the luminal solution, and reduced the H+ content in this fluid. Zinc sulphate pretreatment dose-dependently prevented all these changes. On the other hand, prostaglandin E2 (PGE2) administration only antagonised ethanol ulceration and H+ loss from the chamber; it did not significantly influence the Na+ and K+ fluxes and protein leakage into the luminal solution. It is concluded that the antiulcer mechanisms of zinc sulphate and PGE2 may be different. Protection by the former drug could be due partly to preservation of mucus adhering to the gastric mucosa. The possibility of the membrane-stabilising action of zinc contributing to the observed effects is also discussed.
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PMID:Protection by zinc sulphate against ethanol-induced ulceration: preservation of the gastric mucosal barrier. 294 51

A 35-year-old patient was parenterally fed for a total of 170 days because of a twice reoperated gastric ulcer followed by a gastric-antrum small intestinal fistula. This lead to a complete acute zinc deficiency syndrome with pronounced acrodermatitis enteropathica-like skin changes in the face and the genital region, paronychia, flat blistering on the hands and feet, loss of hair, fingernail ridging (Beau's) and serious physical changes. A dramatic improvement and healing of all these skin changes, the antrum and small intestinal fistula as well as physical disorders occurred after intravenous and subsequent oral intake of zinc.
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PMID:[Zinc deficiency in artificial nutrition]. 312 9

A metallothionein isoform metallothionein-II was isolated from the livers of zinc acetate-treated rats. Metallothionein-II, which showed a single band on polyacrylamide gel electrophoresis, was subjected to two kinds of anti-ulcer screening systems. It was shown that intravenously administered metallothionein-II suppressed the formation of rat water-immersion stress- and HCl-ethanol-induced gastric ulcer significantly. The effect may partly be derived from the zinc contained in the metallothionein-II. However, the effect of metallothionein-II was much stronger than that of an equivalent mole of zinc. Apparently, metallothionein-II had an anti-ulcerogenic activity not based on the effect of intrinsic zinc.
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PMID:Suppression of gastric ulcer induced by stress and HCL-ethanol by intravenously administered metallothionein-II. 334 6


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