In order to determine the role of antioxidative effects of polaprezinc (Z-103) in the mechanism of its anti-ulcer effects, a new chronic ulcer model was produced using Fe2+-ascorbic acid, a free radical generation system, and experiments were conducted to determine characteristics of this model and effects of Z-103 on it. Chronic ulcers were produced by locally injecting 0.4 M Fe2+-ascorbic acid under the serosa in the anterior wall of the glandular stomach. In this model, 3 mg/kg of Z-103 significantly reduced the ulcer area on the 10th and 14th days, and its effects were dose-dependent on the 14th day. In this model, 100 mg/kg of cetraxate HCl and 10 μg/kg of 16, 16-dimethylprostaglandin E2 had almost no effects. However, 200 mg/kg of cimetidine, an H2-antagonist, markedly reduced the ulcer area on the 14th day. On the 11th day, significant increases in TBA-reactive substances and myeloperoxidase activity were observed in ulcerative areas compared to nonulcerative areas. Z-103 (1-10 mg/kg) dose-dependently decreased them, and its effects were significant at 10 mg/kg. While L-carnosine, a related substance of Z-103, had no effect, zinc sulfate and a combination of zinc sulfate and L-carnosine reduced the ulcer area on the 14th day at a dose epuivalent to 3 mg/kg of Z-103. From these findings, free radicals and acid secretion were thought to be involved in the development of chronic ulcer in this model. Z-103 showed marked efficacy in this model, and its effects were thought to be mainly attributable to its antioxidative effects and promoting action of the wound healing of this compound.
|Number of pages||7|
|Publication status||Published - 01-01-1994|
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