Objective：To investigate the effects of luteolin on airway remodeling and the expression of IL-13Rα2 in ｔｈｅ airway ｏｆ chronicity asthmatic mice. Methods：Thirty-two BALB／c mices were randomly divided into four groups. The mouse asthma models（asthma group） were established by sensitization and challenge with ovalbumin（OVA）, eight mices interfered with luteolin 30 min before challenge（luteolin group）, eight mices administrated dexamethasone by intraperitoneal injection 30 min before challenge（dexamethasone group）. The healthy control mice were treated with saline instead of OVA. Lung tissu were collected 24 h after the last challenge. The left lung tissue was enbedded in paraffin and sectioned. Henatoxylin and esin（HE） staining were performed，Histologocial changes were detected. The expressions of genes and their prouducts of IL-13Rα2 in airway were detected using RT-PCR and immunohistochemistry（ISH）. The expressions of genes of TGF-β in lung tissue were detected using RT-PCR. Results：①HE-stained lung tissue showed there were airway remodeling in each group，the thickness of airway in luteolin group was significantly decreased compared with asthma group and increased compared with normal group.②Wat／Pi and Wam／Pi in luteolin group and dexamethasone group were significantly lower than those in asthma group.③RT-PCR showed that expression of IL-13R2mRNA and TGF-β1mRNA in luteolin group and dexamethasone group were significantly lower than those in asthma group. ④ISH Showed that expression of IL-13Rα2 in luteolin group and dexamethasone group were significantly lower than those in asthma group. Conclusion：Luteolin might inhibit the thicking of airway wall and airway smooth muscle proliferation, and inhibit airway remodeling. Its possible mechanisms might be of inhibiting the expression of IL-13Rα2 in the lung tissue.