POSSIBLE MECHANISM OF GASTRIC-MUCOSAL PROTECTION BY EPIDERMAL GROWTH-FACTOR IN RATS

被引:6
作者
AMAGASE, H [1 ]
MURAKAMI, T [1 ]
MISAKI, M [1 ]
HIGASHI, Y [1 ]
HASHIMOTO, K [1 ]
FUWA, T [1 ]
YATA, N [1 ]
机构
[1] WAKUNAGA PHARMACEUT CO LTD,INST MED RES,PHARMACOL LAB,HIROSHIMA 72964,JAPAN
关键词
D O I
10.1016/0024-3205(90)90212-A
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The mechanism of the protection by human epidermal growth factor (hEGF) against the gastric mucosal lesions induced by acidified ethanol was studied in rats. At different times following the subcutaneous administration of hEGF (30 μg/kg), intragastric acidified ethanol (EtOH : 0.125 M HCl = 50 : 50 v/v%) 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 occured about 10 to 30 min after the observed peak plasma concentration of hEGF. Indomethacin and 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 endegeneous prostaglandins, but not sulfhydryls, are the probable mediators for protection against gastric mucosal injury caused by acidified ethanol. © 1990.
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页码:1203 / 1211
页数:9
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