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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 investigate the therapeutic effect of warfarin-based compound DCB-3503 on TNBS-induced ulcerative colitis and its possible mechanism. Methods Twenty-four C57BL / 6 wild-type mice were divided into control (EtOH) group, experimental (TNBS + DMSO) group and treatment group (TNBS + DCB-3503). After 3 days of modeling, the differences of the length of colon, pathological sections and the expression of IFN-γ + inflammatory cells and Tregs in mesenteric lymph nodes were observed. The total proteins of intestinal mucosal epithelial cells (IECs) were isolated and the changes of Treg marker protein Foxp3 were detected by Western blot. Results Compared with the experimental group, the damage in the treatment group was significantly reduced. The number of IFN-γ + cells in the mesenteric lymph nodes was significantly decreased, the number of Treg cells was significantly increased, and the expression of Foxp3 in IECs was significantly increased. Conclusions In ulcerative colitis, DCB-3503 inhibits IFN-γ + inflammatory cells by inducing differentiation of T cells into Foxp3 + Treg cells and ultimately relieves intestinal inflammatory response.