肝脾同治方对哮喘小鼠Th17/Treg及Foxp3/RORγt的影响

Effect of Ganpi Tongzhi Formula on Expression of Th17/Treg and Foxp3/RORγt in Mice with Asthma

目的观察肝脾同治方对哮喘小鼠Th17/Treg及Foxp3/RORγt表达的影响。方法 OVA建立小鼠支气管哮喘气道炎症模型,观察IL-17A、 IL-10、TGF-β1变化及Foxp3/RORγt表达情况。结果与空白组比较,模型组和各药物组支气管肺泡灌洗液IL-17A、TGF-β1值显著升高(P <0.05),IL-10值显著降低(P <0.05);与模型组比较,各药物组IL-17A、TGF-β1值显著降低(P <0.05),IL-10值显著升高(P <0.05)。与空白组比较,模型组Foxp3表达显著降低(P <0.05);与模型组比较,各药物组Foxp3表达量显著升高(P <0.05),其中高剂量组Foxp3表达量最高。与空白组比较,模型组RORγt表达显著升高(P <0.05);与模型组比较,各药物组RORγt表达量显著降低(P <0.05);地塞米松组RORγt表达量最低,高剂量组RORγt表达量低于其余各剂量组。结论肝脾同治方可能通过调节Th17/Treg及Foxp3/RORγt表达,调控Treg/Thl7平衡,起到调节哮喘小鼠慢性气道炎症的作用。

Objective To observe the effects of Ganpi Tongzhi Formula on expression of Th17/Treg and Foxp3/ RORγt in mice with asthma. Methods Model of asthma airway inflammation was established in OVA, changes of IL-17A, IL-10, TGF-β1 level and expression of Foxp3/ RORγt were observed. Results Compared with blank group, values of IL-17A、TGF-β1 were significantly increased ( P < 0.05), and IL-10 value decreased significantly ( P < 0.05) in model group and each drug group. Compared with model group, value of IL-17A、TGF-β1 in each drug group significantly decreased ( P < 0.05), and IL-10 value increased significantly ( P < 0.05). Compared with blank group,expression of Foxp3 was significantly reduced in model group ( P < 0.05). Compared with model group, expression of Foxp3 in each drug group was significantly higher ( P < 0.05), and expression of Foxp3 was the highest in the high- dose group. Compared with blank group, expression of RORγt in model group was significantly increased ( P < 0.05). Compared with model group, expression levels of RORγt were significantly reduced in each drug group (P < 0.05). Among them, expression of RORγt was lowest in the dexamethasone group, and expression of RORγt in t high-dose group was lower than that in the other drug groups. Conclusion Ganpi Tongzhi Formula may regulate expression of Th17/Treg and Foxp3/ RORγt, and regulation of Treg/Th17 balance plays a role in regulating chronic airway inflammation in asthma mice.