目的 观察芦荟大黄素(Aloe-emodin，AE)对三硝基苯磺酸(TNBS)诱导的结肠炎小鼠模型脾脏T细胞亚群的影响。方法 将40只BALB/c小鼠随机分为4组，即乙醇对照组、模型组、AE组及柳氮磺吡啶(SASP)组。后3组以TNBS灌肠制备小鼠结肠炎模型，8 h后给予生理盐水、AE(150 mg·kg-1)或SASP(260 mg·kg-1)灌胃治疗，连续6 d。每天进行疾病活动指数(DAI)评分，6 d后处死小鼠，评估各组结肠组织学损伤指数(TDI)及脏器指数，应用流式细胞仪检测各组小鼠脾脏CD4+/CD8+T细胞及Th1、Th2、Tc1、Tc2细胞亚群的变化情况。结果 AE灌胃治疗可明显降低TNBS结肠炎小鼠的DAI评分和TDI评分(P < 0.01或P < 0.05)；与模型组比较，AE组小鼠脾脏CD4+T淋巴细胞水平明显降低，而CD8+细胞比例升高，CD4+/CD8+比值降低((P < 0.05或P < 0.001)，脾指数下降；AE组小鼠脾脏的Th1细胞、Tc1细胞水平均明显降低(P < 0.05或P < 0.01)，而Th2细胞明显升高(P < 0.001)，Th1/Th2比值、Tc1/Tc2比值也明显降低(P < 0.01)。结论 芦荟大黄素可能通过调节CD4+/CD8+T淋巴细胞亚群的平衡，抑制Th1型/Tc1型细胞分化，诱导以Th2型为主的免疫反应，从而减轻TNBS结肠炎小鼠的炎症病理损伤。

Objective To investigate the effects of aloe-emodin(AE) on splenic T cell subsets in mice with colitis induced by 2，4，6-trinitrobenzenesulfonic acid(TNBS). Methods Forty BALB/C mice were randomly divided into normal control group，model group，AE group and sulfasalazine(SASP) group. Mice in the last three groups were given enema of TNBS to induce colitis，and 8 hours later were given intragastrical administration of normal saline，AE(150 mg·kg-1) or SASP(260 mg·kg-1) respectively once a day for 6 continuous days. Everyday，the disease activity index(DAI) was scored. At the end of medication，colonic tissues damage index(TDI) was evaluated，and the percentages of CD4+/CD8+T cells as well as Th1，Th2，Tc1 and Tc2 cells in mice spleen were analyzed by flow cytometry(FCM). Results DAI and TDI scores in AE group were significantly lower than that of the model group(P < 0.05 or P < 0.01). Meanwhile，the results of FCM analysis showed that the percentage of CD4+T cells，CD4+/CD8+ ratio，spleen index，the percentages of Th1 and Tc1 cells，and the ratio of Th1/ Th2，Tc1/Tc2 were markedly decreased(P < 0.05~P < 0.001)，while the percentages of CD8+ T cells and Th2 cells were increased obviously(P < 0.05~P < 0.001) in the spleen of AE group. Conclusion AE treatment can significantly relieve the inflammatory pathological injury in TNBS-induced colitis of mice，which might be associated with the regulation of CD4+/CD8+T cells balance，inhibition of Th1 /Tc1 differentiation，and induction of Th2 type immunity.

R285.5

国家自然科学基金(30873415)；教育部博士学科点专项科研基金(20124425110010)。