摘要
[目的]探索脾胃湿热型溃疡性结肠炎(UC)的发病机制。[方法]采用高温高湿环境、高脂高糖饮食加免疫法构建脾胃湿热证UC大鼠模型,观察大鼠整体状态、病理变化,检测血清超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平的表达。[结果]与正常对照组相比,脾胃湿热型UC各模型组大鼠的整体状态较差,肉眼可见结肠黏膜糜烂、溃疡形成;镜下呈急慢性炎症表现、溃疡形成,血清中SOD活性下降(P<0.01),MDA水平升高(P<0.05,<0.01)。[结论]氧自由基参与了脾胃湿热型UC的发病过程,外周血SOD、MDA可作为炎症判断指标。
[Objective]To investigate the pathogenesis of ulcerative colitis(UC)with Spleen Stomach Dampness Heat(SSDH)syndrome.[Methods]The rat model was established under the environment of high temperature and high moisture,with diets containing high fat and high sugar,as well as Method of immunity.During the the period,the systemic conditions and pathological changes of rats were monitored,Meanwhile,the activity of SOD and the level of MDA in serum were to be detected.[Results]The systemic conditions was much worse in rats with UC and SSDH syndrome versus the control group.Colon of rats with UC anatomically appeared rottenness and ulceration.The mucosa of UC Under light microscope presented ulceration,acute or chronic inflammatory reaction.In serum,the activity of SOD decreased(P0.01),and the level of MDA increased(P0.05,0.01).[Conclusion]Oxyradical is involved in the pathogensis of UC with SSDH syndrome.The SOD and MDA in serum can be considered as indicators for estimating of inflammation.
出处
《中国中西医结合消化杂志》
CAS
2010年第3期177-179,共3页
Chinese Journal of Integrated Traditional and Western Medicine on Digestion
基金
福建省卫生厅中医药科研项目资助(wzzw0604)