A correlative study of the antiulcer effects of zinc sulphate in stressed rats

Cho, Chi H.; Ogle, C. W.

doi:10.1016/0014-2999(78)90047-x

Cited by 81 publications

(28 citation statements)

References 16 publications

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“…However, any effect of Gamide might be counterbalanced by the direct inhibitory effects of Zn 2C on gastric acid secretion reported by Kirchhoff et al (2011) in isolated gastric glands, and further work will be required to establish the relative importance of the two opposing contributions (Kirchhoff et al 2011). The medical significance of our finding that treatment with Zn 2C ions induces gastrin expression lies in the observation that Zn 2C ions exert a gastro-protective effect (Cho & Ogle 1978). Indeed Zn 2C ions, or compounds containing Zn 2C ions (such as polaprezinc), are used as anti-ulcer drugs and accelerate gastric ulcer healing in humans (Watanabe et al 1995, Opoka et al 2010.…”

Section: Discussionmentioning

confidence: 82%

Zinc ions upregulate the hormone gastrin via an E-box motif in the proximal gastrin promoter

Xiao

Kovac

Chang

et al. 2014

Journal of Molecular Endocrinology

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Gastrin and its precursors act as growth factors for the normal and neoplastic gastrointestinal mucosa. As the hypoxia mimetic cobalt chloride upregulates the gastrin gene, the effect of other metal ions on gastrin promoter activity was investigated. Gastrin mRNA was measured by real-time PCR, gastrin peptides by RIA, and gastrin promoter activity by dual-luciferase reporter assay. Exposure to Zn 2C ions increased gastrin mRNA concentrations in the human gastric adenocarcinoma cell line AGS in a dose-dependent manner, with a maximum stimulation of 55G14-fold at 100 mM (P!0.05). . Deletional mutation of the gastrin promoter identified an 11 bp DNA sequence, which contained an E-box motif, as necessary for Zn 2C -dependent gastrin induction. The fact that E-box binding transcription factors play a crucial role in the epithelial-mesenchymal transition (EMT), together with our observation that Zn 2C ions upregulate the gastrin gene in AGS cells by an E-box-dependent mechanism, suggests that Zn 2C ions may induce an EMT, and that gastrin may be involved in the transition.

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Section: Discussionmentioning

confidence: 82%

Zinc ions upregulate the hormone gastrin via an E-box motif in the proximal gastrin promoter

Xiao

Kovac

Chang

et al. 2014

Journal of Molecular Endocrinology

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“…It has been demonstrated that gastric glandular mucosal mast cell degranulation and the resulting release of histamine are important in the aetiology of stress-induced ulcer formation [9,10], The current findings, therefore, suggest that the anti-ulcer effect of sulphasalazine (table 1), sulphapyridine (ta ble 2) and 5-ASA (table 3) could be due to a combination of inhibition of mast cell de granulation and preservation of mucosal mucus, or to either parameter exerting a sole or a predominant effect; a simultaneous ac tion on both parameters, as shown by the parent drug, antagonised ulceration more strongly. The possibility of inhibition of 5-lipoxygcnasc activity [3], with consequent reduction in leukotriene formation, contrib uting to the observed anti-ulcer action of the drug cannot be excluded, because the leukotrienes have been shown not only to have a histamine-like property but also to be more potent than histamine in several biological systems [13].…”

Section: Discussionmentioning

confidence: 99%

“…The method of staining the mast cells in the gas tric mucosal layer has already been described in detail [10]; only intact metachromatically stained mast cells were counted in 42 adjacent oil immersion fields (magnification X 1,000) covering a l-mm: area im mediately below and parallel to the mucosal surface epithelium.…”

Section: Gastric Mucosal Mast Cell Countsmentioning

confidence: 99%

Inhibition of Stress-Induced Gastric Ulcers by Sulphasalazine and Its Constituents (Sulphapyridine and 5-Aminosalicylic Acid) in Rats

Garg

Cho²,

Ogle³

1990

Pharmacology

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The effects of sulphasalazine and of its major constituents, sulphapyridine and 5-aminosalicylic acid (5-ASA), on gastric ulceration as well as on changes in mast cell counts and mucus levels in the glandular mucosa were examined in restrained rats exposed to 4°C (stress) for 2 h. Sulphasalazine (50, 100, 200 mg/kg), sulphapyridine (31.25, 62.5, 125 mg/kg) or 5-ASA (18.75, 37.5, 75 mg/kg) was injected subcutaneously 0.5 h before stress induction. Cold-restraint stress produced gastric glandular mucosal ulcers which were significantly reduced by all three doses of sulphasalazine and the higher doses of sulphapyridine and 5-ASA. Sulphasalazine prevented mast cell degranulation and increased the amount of mucus adhering to the mucosa. In contrast, the higher doses of sulphapyridine significantly increased only the mucus levels, whereas those of 5-ASA effectively prevented mast cell degranulation. The results show that the total effect of sulphasalazine is approximately equivalent to the summation of the actions of its component doses of sulphapyridine and 5-ASA. It is notable that sulphapyridine itself appears to be biologically active in reducing ulcer severity.

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“…Stomach mucosal erosion size was determined by measuring the lengths of the lesions along their greatest diameters; in the case of petechiae, five of these were taken as the equivalent of a 1 mm lesion. The sum of the lesion lengths, from each rat, was divided by the number of animals in the group and expressed as the mean ulcer index (Cho & Ogle, 1978).…”

Section: Methodsmentioning

confidence: 99%

The protective effects of sulphasalazine against ethanol‐induced gastric damage in rats

Cho

Ogle

Sevilla

1987

British J Pharmacology

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The inhibitory action of sulphasalazine on ethanol‐induced gastric damage was studied in rats. Sulphasalazine (62.5 or 125 mg kg−1, s.c.) did not affect basal gastric acid secretion but increased pepsin output. Ethanol (40% v/v, 10 ml kg−1, p.o.) produced severe gastric glandular mucosal damage and lessened the stomach emptying rate of resin pellets, but it increased the levels of prostaglandin E2 (PGE2)‐like activity in the glandular mucosa. Sulphasalazine markedly prevented ethanol‐induced damage and significantly elevated gastric wall mucus levels both in basal conditions and in the presence of ethanol. Sulphasalazine caused a small insignificant increase in mucosal PGE2 levels in both control and ethanol‐treated rats. The drug significantly increased mucosal PGE2 levels in indomethacin‐treated animals, but did not prevent indomethacin‐induced mucosal damage. Sulphapyridine but not 5‐aminosalicylic acid, constituents of sulphasalazine, showed a similar antilesion action to the parent drug, and prevented gastric wall mucus depletion in ethanol‐treated animals. This study elucidates the protective effects of sulphasalazine against ethanol‐induced gastric lesions. The antagonistic action appears to be mediated, at least partly, through the preservation of gastric wall mucus by sulphapyridine.

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A correlative study of the antiulcer effects of zinc sulphate in stressed rats

Cited by 81 publications

References 16 publications

Zinc ions upregulate the hormone gastrin via an E-box motif in the proximal gastrin promoter

Zinc ions upregulate the hormone gastrin via an E-box motif in the proximal gastrin promoter

Inhibition of Stress-Induced Gastric Ulcers by Sulphasalazine and Its Constituents (Sulphapyridine and 5-Aminosalicylic Acid) in Rats

The protective effects of sulphasalazine against ethanol‐induced gastric damage in rats

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