To investigate the effects of ephedrine on airway inflammation and airway remodeling through transforming growth factor-β1/nuclear factor-κB (TGF-β1/NF-κB) signaling pathway, mice were randomly di-vided into control group, asthma model group, low-dose ephedrine group, high-dose ephedrine group and dexamethasone group, and the mouse model of asthma was constructed by intraperitoneal injection with combination of ovalbumin (OVA) and aluminum hydroxide. Fourteen days after the drug treatment, the airway reactivity of mice was measured by non-invasive pulmonary function tests. The lung histopathology of mice and the proportion of inflammatory cells in bronchoalveolar lavage fluid (BALF) were measured by hematoxy-lin-eosin (HE) staining and Wright-Giemsa staining, respectively. The expression levels of serum OVA-spe-cific immunoglobulin E (IgE) and inflammatory factors in BALF were detected by enzyme linked immunosor-bent assay (ELISA), and the expression levels of TGF-β1/NF-κB pathway-related proteins in lung tissues were analyzed by immunoblot. The results showed that, in asthmatic mice, ephedrine reduced the OVA-specific IgE antibody levels in sera and interleukin (IL)-4, IL-5, IL-6, IL-13 and tumor necrosis factor-α (TNF-α) levels in BALF, and significantly inhibited the expression of TGF-β1/NF-κB pathway-related proteins in lung tissues. The drug could therefore significantly reduce OVA-induced airway hyperresponsiveness and ameliorate lung inflammation.