Possible mechanism of gastric mucosal protection by epidermal growth factor in rats

Journal Article · Mon Jan 01 00:00:00 EST 1990 · Life Sciences; (USA)

DOI:https://doi.org/10.1016/0024-3205(90)90212-A· OSTI ID:6287605

Amagase, Harunobu ^[1]; Murakami, Teruo; Misaki, Masafumi; Higashi, Yutaka; Yata, Noboru ^[2]; Hashimoto, Ken; Fuwa, Tohru ^[3]

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1. Hiroshima Univ. School of Medicine (Japan) Wakunaga Pharmaceutical Co., Ltd., Hiroshima (Japan)
2. Hiroshima Univ. School of Medicine (Japan)
3. Wakunaga Pharmaceutical Co., Ltd., Hiroshima (Japan)

At different times following the subcutaneous administration of hEGF, intragastric acidified ethanol was administered to induce an experimental gastric mucosal lesion. Mean length of the lesion in the gastric mucosa was used as a lesion index. Extravasation of intraveneously injected Evans blue into the gastric wall and gastric contents was used as an indicator of vascular permeability. Pretreatment with hEGF decreased both the gastric mucosal lesions and the increase of vascular permeability caused by acidified ethanol with similar time profiles relative to pretreatment with hEGF. Maximal protective actions of hEGF occurred about 10 to 30 min after the observed peak plasma concentration of hEGF. Indomethacine and {und N}-ethylmaleimide, but not iodoacetamide, blocked the protective action of hEGF, indicating that endogeneous prostaglandins and/or sulfhydryls may participate in the protective action of hEGF. The content of endogeneous nonprotein sulfhydryls in the gastric mucosa decreased markedly after acidified ethanol. However, pretreated hEGF did not restore the sulfhydryl contents. Thus, it seemed that endogenous prostaglandins, but not sulfhydryls, are the probable mediators for protection against gastric mucosal injury caused by acidified ethanol.

• OSTI ID: 6287605
• Journal Information: Life Sciences; (USA), Vol. 47:14; ISSN 0024-3205
• Country of Publication: United States
• Language: English

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