人结肠粘膜Mr40KD蛋白的提取、纯化及免疫学特性鉴定

目的 探索非特异性溃疡性结肠炎(UC)血清学诊断方法。方法 采用DE-52离子交换层折及cNBr-Sepharose 4B亲和层析技术从人结肠粘膜组织中提取一种蛋白组分，经10％SDS-PAGE、IEF、CIE及Westem blot技术，对该蛋白分子量、等电点及免疫学等进行鉴定。结果 产物PI为5．8，分子量为40KD，免疫学鉴定发现其主要与UC患者血清起反应。结论 人结肠40KD蛋白可能是UC的一种自身抗原，血清中ACA可以作为UC的一个特异性指标。     

Inflammatory bowel disease unclassified

Objective  

Inflammatory bowel diseases (IBDs) are idiopathic, chronic, and inflammatory intestinal disorders. The two main types, ulcerative colitis (UC) and Crohn’s disease (CD), sometimes mimic each other and are not readily distinguishable. The purpose of this study was to present a series of hospitalized cases, which could not initially be classified as a subtype of IBD, and to try to note roles of the terms indeterminate colitis (IC) and inflammatory bowel disease unclassified (IBDU) when such a dilemma arises.     

Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats

The histopathological features and the associated clinical findings of ulcerative colitis (UC) are due to persistent inflammatory response in the colon mucosa. Interventions that suppress this response benefit UC patients. We tested whether sodium arsenite (SA) benefits rats with dextran sulfate sodium (DSS)-colitis. The DSS-colitis was induced by 5% DSS in drinking water. SA (10 mg/kg; intraperitoneally) was given 8 h before DSS treatment and then every 48 h for 3 cycles of 7,14 or 21 d. At the end of each cycle rats were sacrificed and colon sections processed for histological examination. DSS induced diarrhea, loose stools, hemoccult positive stools, gross bleeding, loss of body weight, loss of epithelium, crypt damage, depletion of goblet cells and infiltration of inflammatory cells. The severity of these changes increased ir the order of Cycles 1,2 and 3. Treatment of rats with SA significantly reduced this severity and improved the weight gain.