Abstract: OBJECTIVE To study the effects of praeruptorin C on the imbalance of Th17/Treg in a mouse model of allergic asthma. METHODS BALB/c mice were sensitized and challenged by OVA to induce airway inflammation, and administered intragastrically with praeruptorin C at different doses. Airway responsiveness was measured by a lung function analysis systems. The number of total and differential leukocytes in BALF was counted using a hemocytometer or Diff-Quick-stained smears. The pathological inspection of lung tissue was analyzed by hematoxylin-eosin staining. Levels of cytokine and inflammatory mediators in BALFs or serum were measured by enzyme-linked immunosorbent assay. Numbers of CD4⁺ T cells in spleen was analyzed by flow cytometry. The expression of Foxp3 mRNA in spleen was detected by reverse transcription polymerase chain reaction. RESULTS Compared with control group, the model group exhibited obvious airway inflammation and hyperreactivity(P<0.05 or P<0.01), the levels of IgE and IL-17 were significantly increased(P<0.01), levels of IL-10 and TGF-β1 was significantly decreased(P<0.01), the percentages of CD4⁺CD25⁺Foxp3⁺ regulatory T cell among the CD4⁺ T cells were significantly decreased(P<0.01), and the expression of Foxp3 mRNA was significantly decreased(P<0.01). Compared with the model group, the group of praeruptorin C exhibited ease of airway inflammation, airway hyperreactivity in the middle and high dose of praeruptorin C groups were obviously suppressed as the dose of acetylcholine chloride were more than 10 mg·kg^-1, the groups of praeruptorin C reduced the levels of IgE significantly(P<0.01) and increased the levels of IL-10, TGF-β1(P<0.05 or P<0.01), the middle and high dose of praeruptorin C reduced the levels of IL-17 significantly(P<0.01), the groups of praeruptorin C increased the percentages of CD4⁺CD25⁺Foxp3⁺ regulatory T cell and the expression of Foxp3 mRNA(P<0.05 or P<0.01). CONCLUSION Praeruptorin C efficiently regulates the imbalance of Th17/Treg to balance a mouse model of allergic airway inflammation.