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氧自由基在禁食限制应激诱导的小鼠胃黏膜损伤发病机制中的作用。

The role of oxygen radicals in the pathogenesis of gastric mucosal lesions induced in mice by feeding-restriction stress.

作者信息

Nakamura K, Aoike A, Rokutan K, Hosokawa T, Koyama K, Kawai K

机构信息

Department of Preventive Medicine, Kyoto Prefectural University of Medicine, Japan.

出版信息

Scand J Gastroenterol Suppl. 1989;162:47-50. doi: 10.3109/00365528909091122.

DOI:10.3109/00365528909091122
PMID:2595306
Abstract

To investigate the role of oxygen radicals in the pathogenesis of gastric mucosal lesions induced by psychological stress, we exposed 3-mo-old C3H mice to feeding-restriction stress for 1 to 5 days. Serial changes in the activities of antioxidant enzymes in the gastric mucosa, together with O2- production by macrophages, were measured. The stress increased the plasma cortisol level and started to produce acute gastric lesions (AGL) on the 2nd day. Before the development of AGL, the activity of superoxide dismutase in the gastric mucosa had already decreased and the ability of O2- production by macrophages was enhanced from the 1st day. This suggests that oxygen radicals play some role in the development of AGL induced by the stress.

摘要

为了研究氧自由基在心理应激诱导的胃黏膜损伤发病机制中的作用,我们将3月龄的C3H小鼠置于进食限制应激环境中1至5天。检测了胃黏膜中抗氧化酶活性的系列变化以及巨噬细胞产生超氧阴离子的情况。应激使血浆皮质醇水平升高,并在第2天开始产生急性胃损伤(AGL)。在AGL出现之前,胃黏膜中超氧化物歧化酶的活性已经降低,并且从第1天起巨噬细胞产生超氧阴离子的能力就增强了。这表明氧自由基在应激诱导的AGL发生过程中发挥了一定作用。

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