目的 从效应T细胞活化的源头Treg/Th17入手，探讨溃结灵调节Th17和Treg的平衡转化机制，揭示溃结灵治疗溃疡性结肠炎（UC）的深层次作用机理及作用靶点。方法 采用2，4，6-三硝基苯磺酸（TNBS）（25 g•L-1 TNBS+50 %的乙醇）诱导复制UC大鼠模型，并随机分为模型组，溃结灵高、中、低剂量组，阳性药柳氮磺胺吡啶（SASP）组，另取12只SD大鼠设为正常组。流式细胞术检测大鼠外周血中Treg细胞和Th17细胞占总CD4+T细胞百分比及计算Treg/Th17之比。结果 模型组Treg/Th17之比，较正常组显著降低（P＜0.01），溃结灵高、中、低剂量组以及柳氮磺胺吡啶组Treg/Th17之比与模型组比较均有显著升高（P＜0.05，P＜0.01）。结论 溃结灵对TNBS诱导的实验性溃疡性结肠炎大鼠有明显的治疗作用，其作用机制可能与提高外周血CD4+ Foxp3+Treg细胞比例和降低CD4+IL-17A+ Th17细胞比例，进而恢复机体Treg/Th17平衡有关。

Objective To observe the effect of Kuijieling（KD） on regulating the balance of Treg/Th17，which reflect the activation of effector T cells，and to reveal the therapeutic mechanism of KD for ulcerative colitis（UC） and the action target. Methods Trinitro-benzene-sulfonic acid（TNBS） 25 g•L-1 together with 50 % of ethanol was used for the establishment of UC rat model. The proportion of Treg and Th17 cells in peripheral blood CD4+T cells and the ratio of Treg/Th17 were detected by flow cytometry. Results The ratio of Treg/Th17 in the model group was lower than that of the blank control group（P＜0.01），while was higher in high-，medium- and low-dosage KD groups and salicylazosulfapyridine（SASP） group than that of the model group（P＜0.05，P＜0.01）. Conclusion KD shows obvious effect for the treatment of rats with TNBS-induced UC，and the therapeutic mechanism may be related with the regulation of Treg/Th17 balance through increasing the proportion of CD4+Foxp3+Treg cells and lowering the proportion of CD4+IL-17A+ Th17 cells in peripheral blood of UC rats.

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国家自然科学基金（81373798）；广州中医药大学中医内科学国家重点学科专项；中央财政支持地方高校发展专项资金项目“重大难治性脾胃病防治协同创新平台”（财教2013-338号）。