中药灌肠1号对小鼠结肠炎CD4^＋CD25^＋免疫作用的研究

Effects and mechanism of CD4^+ CD25^+ regulatory T cells in mouse experimental colitis treated by CLYSTER No.1

目的:探讨CD4^+CD25^+调节性T细胞(Tregs)在2,4-二硝基氯苯(DNCB)和醋酸(AA)复合法诱发的小鼠溃疡性结肠炎中的变化规律及中药灌肠1号治疗的作用机制。方法:建立DNCB+AA复合法诱发的小鼠溃疡性结肠炎模型,设立正常对照、模型对照、柳氮磺氨吡啶(SASP)和中药灌肠1号治疗共4组,用流式细胞仪检测各组外周血、肠系膜淋巴结CD4^+CD25^+Tregs细胞的变化以及结肠组织病理学改变。结果:建模后1～2周,模型组外周血和肠系膜淋巴结的CD4^+CD25^+Tregs细胞数量较正常组明显下降,而使用SASP和中药灌肠Ⅰ号治疗后该细胞亚群明显高于模型组。结论:具有较强免疫抑制作用的CD4^+CD25^+Tregs细胞亚群在小鼠实验性溃疡性结肠炎的发病及病情转归中可能具有重要免疫调节作用,中药灌肠1号通过调节Tregs细胞的数量对溃疡性结肠炎发挥治疗作用。

Objective： To explore the effects and mechanism of CD4^＋ CD25^ ＋ regulatory T cells （Tregs） in mouse experimental colitis treated by CLYSTER No. 1. Method： The mouse model of experimental colitis was established by dinitrochlorobenzene （DNCB）-acetic acid （AA） in mice DNCB and AA. Aduh KM mouse were randomly divided into four groups, normal control group, experimental colitis model group, SASP and Chinese medicine therapeutic groups. Proportion of CD4^＋ CD25^＋ Tregs in peripheral blood （PB） and mesenteric lymph node （MLN） was estimated by flow cytometry at the end of one or two week after treating with SASP and CLYSTER No. 1. Result：The model of experimental colitis in mouse was successfully established. Compared with normal control group, the proportion of CD4^＋ CD25^＋ Tregs was markedly decreased in PB and MLN of model control group of experimental colitis. But it was significantly increased in therapeutic groups of SASP and CLYSTER No. 1, and their CD4^＋ CD25^＋ Tregs in PB and MLN were much more than the model control group at the end of one or two weeks after treating with SASP and CLYSTER No. 1. Conclusion： CD4^＋ CD25^＋ Tregs with strong immune suppression could play a central role in the initiation and development of mouse experiment colitis, and the CLYSTER No. 1 might exert its therapeutic effects on UC by the regulation of number and function of CD4^＋ CD25^＋ Tregs.