Objective:San’ao Decoction(三拗汤,SAD),as a representative Chinese medicine(CM)formula, was chosen to evaluate the effect of airway inflammation and hyperresponsiveness on the lipopolysaccharide (LPS)enhanced asthma model.Methods:The asthma model was reproduced in the Balb/C mice sensitized by ovalbumin(OVA),challenged by OVA and LPS.After Balb/C mice’s administration of a dose(0.0024 g/kg)of dexamethasone acetate,and three doses(2.2 g/kg,4.4 g/kg and 8.8 g/kg)of SAD,airway inflammation and responsiveness were observed.The airway inflammation was detected by counting bronchoalveolar lavage fluid (BALF)cells and lung histopathology.Also,differential expressions of interferon-r(IFN-γ),interleukin-4(IL-4), and IL-5 in the supernatants of BALF were examined.The changes in airway responsiveness indicated by lung resistance(R_L)and stimulated by acetylcholine(Ach)were determined.Results:Small-dose SAD hardly inhibit airway inflammation or hyperresponsiveness in the LPS-enhanced asthma,while medium-dose and high-dose SAD significantly inhibited the airway hyperresponsiveness,and to some extent,reduced airway inflammation. Meanwhile,the small-dose,medium-dose,and high-dose SAD promoted Th1-type cytokines(IFN-γ)and reduced Th2-type cytokines(IL-4,IL-5)to different extents,which led to a Th1/Th2 balance.Conclusion:SAD has a good therapeutic effect on airway hyperresponsiveness in the LPS-enhanced asthma model,but its definite influence on airway inflammation is not remarkable. Objective: San’ao Decoction, as a representative Chinese medicine (CM) formula, was chosen to evaluate the effect of airway inflammation and hyperresponsiveness on the lipopolysaccharide (LPS) enhanced asthma model. Methods: The asthma model was reproduced in the Balb / C mice sensitized by ovalbumin (OVA), challenged by OVA and LPS. After Balb / C mice’s administration of a dose (0.0024 g / kg) of dexamethasone acetate, and three doses (2.2 g / kg, airway inflammation and responsiveness were observed. Airway inflammation was detected by counting bronchoalveolar lavage fluid (BALF) cells and lung histopathology. Also, differential expressions of interferon-r (IFN-γ) , interleukin-4 (IL-4), and IL-5 in the supernatants of BALF were examined. Changes in airway responsiveness indicated by lung resistance (R_L) and stimulated by acetylcholine (Ach) were determined. Results: Small-dose SAD hardly inhibit airway inflammation or hyperresponsiveness in the LPS-enhanced asthma, wh ile medium-dose and high-dose SAD significantly inhibited the airway hyperresponsiveness, and to some extent, reduced airway inflammation. However, the small-dose, medium-dose, and high-dose SAD promoted Th1-type cytokines and reduced Th2-type cytokines (IL-4, IL-5) to different extents, which led to a Th1 / Th2 balance. Confluence: SAD has a good therapeutic effect on airway hyperresponsiveness in the LPS-enhanced asthma model, but its definite influence on airway inflammation is not remarkable.