为探讨黄芪甲苷Ⅳ（astragaloside Ⅳ， AST Ⅳ）对哮喘小鼠免疫失衡的调节机制，用卵清蛋白（ovalbumin， OVA）诱导小鼠支气管哮喘模型，随机分为对照组、模型组、AST Ⅳ治疗组和地塞米松治疗组。HE染色观察肺组织病理改变；ELISA检测肺组织匀浆中IFN-γ、IL-5、IL-13、IL-17A及TGF-β的含量变化；RT-PCR检测脾脏中转录因子T-bet、GATA-3、STAT-6、RORγt和Foxp3 mRNA的表达水平。结果显示，AST Ⅳ作用后小鼠肺部炎症细胞浸润及气道上皮细胞损伤明显改善；IL-5、IL-13和IL-17A的表达水平明显低于模型组（P ＜ 0.05），而对IFN-γ和TGF-β没有显著作用；AST Ⅳ能显著抑制STAT-6 mRNA的表达（降低2.65倍），同时对GATA-3（降低1.82倍）和RORγt（降低2.22倍）的表达也有抑制作用；但对Foxp3和T-bet mRNA表达无显著影响。研究表明，AST Ⅳ主要通过显著抑制Th2转录因子表达来抑制炎性因子IL-5、IL-13以及IL-17A的产生，从而改善哮喘模型小鼠肺部炎症程度。故AST Ⅳ可能是一种哮喘治疗新的药物活性成分。

We aimed to explore the mechanisms of how AST Ⅳ suppresses airway inflammation in bronchial asthma. Ovalbumin-induced mouse asthma model was established. A total of 40 BALB/c male mice were selected and divided into control, asthma, AST Ⅳ and dexamethasone groups. HE staining was conducted to observe the pulmonary pathological changes. ELISA was adopted for measuring the levels of IFN-γ, IL-5, IL-13, IL-17A and TGF-β, and RT-PCR for mRNA measurement of the main transcriptional factors T-bet, GATA-3, STAT6, RORγt and Foxp3. Compared with the control group, the asthma group had irregular tissue structure and severe inflammation. AST Ⅳ strongly ameliorated injury of airway epithelial cells, diminished accumulation of inflammatory cells, and reduced levels of Th2 cytokines IL-5, IL-13 and IL-17A in the lung homogenate (P ＜ 0.05). But AST Ⅳ had no significant effect on IFN-γ and TGF-β. AST Ⅳ exerted immunomodulatory effects by suppressing production of Th2 cytokines IL-5 and IL-13 through downregulation of STAT-6 mRNA (2.65 folds) and GATA-3 mRNA (1.82 folds), meanwhile, AST Ⅳ also suppressed expression of RORγt mRNA (2.22 folds), but had no effect on T-bet and Foxp3 mRNA. These results suggest that the anti-asthmatic activity of AST Ⅳ may occur by the suppression of IL-5, IL-13 and IL-17A production through inhibition of the main transcriptional of factors of Th2 cell, resulting in the improvement of allergic asthma. AST Ⅳ could be a new therapeutic component for allergic asthma.