摘要
目的探讨娃儿藤碱类化合物DCB-3503对三硝基苯磺酸(TNBS)诱导溃疡性结肠炎的治疗作用及可能的作用机制。方法选用C57BL/6野生型小鼠24只,分为对照(EtOH)组、实验(TNBS+DMSO)组、治疗(TNBS+DCB-3503)组。造模3 d后,观察各组间结肠长度、病理切片以及肠系膜淋巴结中IFN-γ+炎症性细胞和调节性T细胞(Treg)的差异。分离肠黏膜上皮细胞(IECs)总蛋白,Western blot检测Treg标志蛋白Foxp3的变化。结果治疗组损伤较实验组明显减轻,其肠系膜淋巴结中IFN-γ+细胞显著减少,Treg细胞显著增多,且IECs中Foxp3表达明显上调。结论在溃疡性结肠炎中,DCB-3503通过诱导T细胞分化为Foxp3+Treg细胞,从而抑制IFN-γ+炎症性细胞发挥作用,最终缓解肠道的炎症反应。
Objective To evaluate the protective effect of tylophorine DCB-3503 on trinitrobenzene sulfonic acid ( TNBS) induced ulcerative colitis and the possible molecular mechanism. Methods 24 C57BL/6 wild-type mice were di- vided into three groups : EtOH group, TNBS + DMSO group and TNBS + DCB-3503 group. Three days after the model was set up, the mice were killed and colon length, histological section, patterns of IFN-γ inflammatory cells and Treg cells were examined. Besides, the expression of Foxp3 in IECs was detected using Western blot. Results Compared with TNBS + DMSO group, DCB-3503 treatment group displayed remarkably improved clinical symptoms. Percentage of IFN-,,/~ inflammatory cells in mesenteric lymph node was significantly decreased in TNBS + DCB-3503 group. Meanwhile the percentage of Treg cells in mesenteric lymph node and the expression of Foxp3 in intestinal epithelial cells (IECs) were significantly increased after DCB-3503 treatment. Conclusion The increase of Treg cells and de- crease of IFN-γ inflammatory cells in DCB-3503 treatment group suggest that DCB-3503 can ameliorate the ulcerative colitis induced by TNBS via the growing number of Foxp3 Treg cells and their suppression on IFN-γ, inflammatory cells.
出处
《山东大学学报(医学版)》
CAS
北大核心
2012年第10期81-85,共5页
Journal of Shandong University:Health Sciences