共刺激分子及黏附分子在大鼠实验性结肠炎中的表达研究

Costimulatory molecules and adhesion molecules in experimental colitis of rats

目的探讨共刺激分子及黏附分子在大鼠实验性结肠炎发病中的作用。方法建立三硝基苯磺酸诱导的实验性结肠炎大鼠模型,并予以泼尼松或柳氮磺胺吡啶治疗,设立正常对照及未治疗组对照,进行组织学评分;流式细胞仪检测各组外周血、脾脏和结肠上皮内单个核细胞CD28、CTLA-4及CD11b的表达。结果实验性结肠炎大鼠在外周血、脾脏和结肠表达CD11b、CD28及CTLA-4均较正常对照组升高,有统计学意义,而经泼尼松或柳氮磺胺吡啶治疗后在结肠的CD11b和CD28的表达有所回落,而CTLA-4升高更加明显,均有统计学意义。结论黏附分子可能参与了大鼠实验性结肠炎的发生,CD28与CTLA-4表达失调可能是发病机制之一,泼尼松和柳氮磺胺吡啶的治疗机制可能与共刺激分子及黏附分子有关。

Objective： To investigate costimulatory molecules and adhension molecules in the pathogenesis of experimental colitis in rats. Methods： Models of experimental colitis were established by enema with trinitrobenzenesulphonic acid. Prednisolone or salicylazosulfapyridine was given as treatment. Nomal rat and untreated colitis rat groups were set up as controls. Histological scoring was performed. Expression of CD11 b, CD28 and CTLA-4 were detected by flow cytometry in peripheral blood, spleen and intraepithelial mononuclear cells of colon. Results：Expressions of CD11b,CD28 and CTLA-4 were high in experimental colitis. CD11b and CD28 decreseased after treatment of prednisolone or salicylazosulfapyridine,while CTLA-4 increased further,which were significant statistically. Conclusion：Adhesion molecules may have a role in the pathogenesis of experimental colitis. The dysregulation of CD28 and CTLA-4 may be one of the mechanisms in IBD. The mechanisms of prednisolone and salicylazosulfapyridine may be associated with costimulatory molecules and adhension molecules.