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大鼠细菌肽聚糖 - 多糖诱导的结肠炎期间结肠核因子 - κB表达的时间进程

Time course of colonic nuclear factor-kappa B expression during bacterial peptidoglycan-polysaccharide-induced colitis in rats.

作者信息

Fitzpatrick Leo R, Wang Jian, Le Truc, Calingasan Noel

机构信息

Gastrointestinal Inflammation Department, Maryland Research Laboratories, Otsuka Maryland Research Institute, Rockville, Maryland 20850, USA.

出版信息

Dig Dis Sci. 2003 Apr;48(4):775-82. doi: 10.1023/a:1022853213009.

Abstract

Nuclear factor-kappa B has been proposed to play a role in the pathogenesis of bacterial peptidoglycan-polysaccharide-induced colitis. However, its colonic expression has not been defined in detail. The primary aim of this study was to profile this expression in the rat colon. Peptigoglycan-polysaccharide was administered to the rat colon by direct intramural injections. Gross colonic injury was determined at various time points. Concomitantly, colonic nuclear factor-kappa B was measured by an electrophoretic mobility shift assay and by immunohistochemistry. Gross colonic injury and colonic nuclear factor-kappa B expression showed similar time courses following peptigoglycan-polysaccharide administration. Peak colonic injury and nuclear factor-kappa B expression were found on day 21. Nuclear factor-kappa B was mainly expressed in submucosal inflammatory cells. In conclusion, the administration of bacterial peptidoglycan-polysaccharide to the rat colon caused a chronic colitis, which was characterized by up-regulated colonic nuclear factor-kappa B.

摘要

核因子-κB被认为在细菌肽聚糖-多糖诱导的结肠炎发病机制中起作用。然而,其在结肠中的表达尚未得到详细界定。本研究的主要目的是分析其在大鼠结肠中的表达情况。通过直接壁内注射将肽聚糖-多糖注入大鼠结肠。在不同时间点测定结肠大体损伤情况。同时,通过电泳迁移率变动分析和免疫组织化学法检测结肠核因子-κB。给予肽聚糖-多糖后,结肠大体损伤和结肠核因子-κB表达呈现相似的时间进程。在第21天发现结肠损伤和核因子-κB表达达到峰值。核因子-κB主要表达于黏膜下炎症细胞。总之,向大鼠结肠给予细菌肽聚糖-多糖可导致慢性结肠炎,其特征为结肠核因子-κB上调。

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