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巯基阻断剂诱导的大鼠结肠炎:胸腺和结肠黏膜的免疫变化

Sulfhydryl blocker-induced colitis in the rat: immunological changes in thymus gland and colonic mucosa.

作者信息

Suzuki H, Hibi T, Oda M, Hosoda Y, Mori M, Miura S, Tanaka S, Watanabe M, Tsuchiya M

机构信息

Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.

出版信息

J Gastroenterol Hepatol. 1994 Nov-Dec;9(6):544-50. doi: 10.1111/j.1440-1746.1994.tb01558.x.

Abstract

The study was designed to examine the changes of thymus in sulfhydryl blocker-induced colitis. We used N-ethylmaleimide (NEM) as sulfhydryl blockers. Fasted male Sprague-Dawley rats were given 3% NEM in 1% methyl cellulose into the colon. N-ethylmaleimide treatment caused severe diarrhoea with bleeding for the first 7 days. At autopsy, adhesions, colon dilatation, and single or multiple erosions and ulcers were observed. Time-course studies revealed that the lesions were most extensive and severe 3 or 7 days after the administration of NEM. Histological examination of colon on the 3rd day after NEM treatment demonstrated mucosal erosion, oedema and extensive infiltration of neutrophils. The mucosal lesions extended into the submucosa and muscle on the 7th day after NEM treatment. Immunohistochemical studies showed that T cells and macrophages were markedly increased in the lamina propria of colonic mucosa. After 3 weeks, the infiltration of chronic inflammatory cells was observed and regeneration of the mucosa was noticed. The thymus gland was significantly decreased in weight and size on the 3rd day after NEM treatment, but the weight loss of thymus gland was regained in 3 weeks. Transient atrophy of thymus gland was noticed in this colitis model. The phenotypes of thymocytes were not influenced by NEM treatment. It is concluded that the thymus abnormalities in human ulcerative colitis are not induced in this animal model and that other chronic models are necessary for the elucidation of the immunological abnormalities, including thymus abnormalities.

摘要

本研究旨在探讨巯基阻断剂诱导的结肠炎中胸腺的变化。我们使用N-乙基马来酰亚胺(NEM)作为巯基阻断剂。将禁食的雄性Sprague-Dawley大鼠经结肠给予1%甲基纤维素中的3% NEM。N-乙基马来酰亚胺处理在最初7天导致严重腹泻伴出血。尸检时,观察到粘连、结肠扩张以及单个或多个糜烂和溃疡。时间进程研究表明,在给予NEM后3天或7天,病变最为广泛和严重。NEM处理后第3天结肠的组织学检查显示黏膜糜烂、水肿和中性粒细胞广泛浸润。NEM处理后第7天,黏膜病变扩展至黏膜下层和肌肉层。免疫组织化学研究表明,结肠黏膜固有层中的T细胞和巨噬细胞明显增加。3周后,观察到慢性炎症细胞浸润,并注意到黏膜再生。NEM处理后第3天,胸腺重量和大小显著降低,但3周后胸腺重量恢复。在该结肠炎模型中观察到胸腺短暂萎缩。NEM处理未影响胸腺细胞的表型。结论是,在该动物模型中未诱导出人类溃疡性结肠炎中的胸腺异常,并且需要其他慢性模型来阐明包括胸腺异常在内的免疫异常。

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