复方青黛颗粒治疗溃疡性结肠炎的机制  

Mechanisms of Qingdaikeli′s anti-ulcerative colitis effects

作　　者：邹莉波[1] 刘艳[2] 先宇飞[1] 吴琦[1] 杨新爱[1] 杜立阳[2] 

机构地区：[1]沈阳药科大学药学院,辽宁沈阳110016 [2]中国医科大学第一临床医院,辽宁沈阳110001

出　　处：《沈阳药科大学学报》2006年第2期119-122,128,共5页Journal of Shenyang Pharmaceutical University

基　　金：辽宁省自然科学基金资助项目(972261);沈阳市社会发展基金资助项目(9849340513)

摘　　要：目的探讨复方青黛颗粒抗实验性溃疡性结肠炎(UC)的作用机制。方法用三硝基苯磺酸(TNBS)法制备大鼠溃疡性结肠炎模型,采用酶联免疫吸附(ELISA)方法测定血清中肿瘤坏死因子(TNF-α)、白细胞介素(IL 1βI、L 4)含量;用流式细胞仪测定结肠组织中CD54阳性细胞率。结果复方青黛颗粒300、600、1 200 mg.kg-1连续灌胃3周,剂量依赖性地降低大鼠血清TNFα及IL 1β水平,升高血清IL 4水平;剂量依赖性地降低动物结肠组织CD54阳性细胞百分率。结论复方青黛颗粒抗实验性溃疡性结肠炎的作用机制可能与下调CD54的过度表达和调节IL 1βI、L 4及TNFCYα水平有关。Objective To investigate the mechanisms of Qingdaikeli（QDK, traditional Chinese medicines）. Methods The rat UC model established in our study was induced by TNBS. Serum TNF-α, IL-1β and IL-4 levels were determined by enzyme-linked immunosorbent assay. Content of adhesion molecule CD54 was determined with flow cytometer. Results Compared with the model group, the serum level of TNF-α of QDKtreated rats was significantly decrease on the seventh day. And the administration of QDK markedly decreased the levels of serum IL-1β while the level of serum IL-4 increased compared with model group. The levels of colonic CD54 on the twentieth day was markedly decreased after the administration of QDK. Conclusions QDK has obvious protective effects against UC in experimental animals.

关 键 词：复方青黛颗粒 溃疡性结肠炎 肿瘤坏死因子 白细胞介素-1Β 白细胞介素-4 CD54 

分 类 号：R96[医药卫生—药理学] R94[医药卫生—药学]