Nakano S, Ohara S, Kubota T, Saigenji K, Hotta K
Department of Internal Medicine, School of Medicine, Kitasato University.
Nihon Shokakibyo Gakkai Zasshi. 1998 Jun;95(6):513-23.
We investigated the quantitative changes in colonic mucins of rats with colitis. Male Wistar rats were treated with dextran sodium sulfate (DSS) or N-ethylmaleimide (NEM) to induce colitis. Both DSS and NEM caused depletion of goblet cells, infiltration of inflammatory cells and erosion at the colonic mucosa around the anus. Though the goblet cells decreased, colonic mucins increased in the distal colon. These phenomena may explain the clinical features of human ulcerative colitis, namely the goblet cell depletion and the mucous stool. The increase of colonic mucins may be a compensatory function of the colon tissue in response to the localized decrease of mucin production.
我们研究了结肠炎大鼠结肠黏蛋白的定量变化。雄性Wistar大鼠用葡聚糖硫酸钠(DSS)或N-乙基马来酰亚胺(NEM)处理以诱导结肠炎。DSS和NEM均导致杯状细胞减少、炎性细胞浸润以及肛门周围结肠黏膜糜烂。尽管杯状细胞减少,但结肠远端的结肠黏蛋白增加。这些现象可能解释了人类溃疡性结肠炎的临床特征,即杯状细胞减少和黏液便。结肠黏蛋白的增加可能是结肠组织对黏蛋白产生局部减少的一种代偿功能。