蒙药嘎日迪散对溃疡性结肠炎大鼠Th1细胞和Th17细胞的影响

目的探讨蒙药嘎日迪散对溃疡性结肠炎(UC)大鼠Th1细胞和Th17细胞的影响。方法将Wistar大鼠随机分为正常组、UC模型组、嘎日迪散低剂量组、嘎日迪散中剂量组、嘎日迪散高剂量组、柳氮磺吡啶组和补脾益肠丸组,采用免疫法加2,4,6-三硝基苯磺酸乙醇诱导UC模型。嘎日迪散低、中、高剂量组(1.76、3.51、7.02 g/kg),柳氮磺吡啶组(0.36 g/kg)和补脾益肠丸组(1.62g/kg)分别灌胃相应药物4周后,取外周血检测指标。采用流式细胞术观察全血中Th1细胞/Th17细胞(Th1/Th17),ELISA法检测血清中转化生长因子β(TGF-β)、白细胞介素6(IL-6)、白细胞介素17(IL-17)、干扰素γ(IFN-γ)的含量。结果嘎日迪散中、低剂量和柳氮磺吡啶能显著降低UC大鼠血清中TGF-β,各药物均能显著降低UC大鼠血清中IL-6、IL-17的含量(P0.05)、升高IFN-γ的含量(P0.05),升高Th1/Th17值(P0.05)。结论嘎日迪散调节UC大鼠体内Th0细胞的分化方向,恢复Th1/Th17的平衡可能是其治疗UC的机制之一。

Influence of Mongolia medicine-Garidi San on Th1 and Th17 in rats with ulcerative colitis

Objective To discuss the influence of Mongolia medicine-Garidi San on helper T cell 1 (Th1) and helper T cell 17 (Th17) in rats with ulcerative colitis (UC).Methods All rats were randomly divided into normal group, model group, low-dose Garidi San group (low-dose group), mid-dose Garidi San group (mid-dose group), high-dose Garidi San group (high-dose group), sulfasalazine group (SSZ group) and Bupi Yichang Wan group.The UC model was induced and established by using immune method and TNBS.Garidi San was orally given to, respectively, low-dose group (1.76 g/kg), mid-dose group (3.51 g/kg) and high-dose group (7.02 g/kg), SSZ was given to SSZ group (3.60 g/kg), and Bupi Yichang Wan was given to Bupi Yichang Wan group (1.62 g/kg).After 4 weeks the samples of peripheral blood were collected from all groups.The ratio of Th1 to Th17 (Th1/Th17) in peripheral blood was observed by using flow cytometry, and levels of PB transforming growth factor β (TGF-β), interleukin-6 (IL-6), interleukin-17 (IL-17) and interferon-γ (IFN-γ) were detected by using enzyme-linked immunosorbent assay (ELISA).Results The level of TGF-β was decreased significantly in mid-dose group, low-dose group and SSZ group.The levels of serum IL-6 and IL-17 were decreased significantly(P<0.05), level of IFN-γ was increased (P<0.05), and Th1/Th17 was increased (P<0.05) in all medication groups.Conclusion Garidi San can regulate the differentiation direction of helper T cell 0, and recover the balance of Th1/Th17 in UC rats, which may be one of mechanisms of Garidi San curing UC.