Objective:To observe the effects of chrysin on the expression of nuclear factor (NF)-κB in lung tissues in a murine model of asthma. Methods: Twenty-four female BALB/c mice were randomly divided into 4 groups, including control group, asthma group, chrysin group and budesonide group. BALB/c mice were sensitized by intraperitoneal injection and challenged via the airway with ovalbumin(OVA). Mice in the chrysin group were intragastrically administered with chrysin (50 mg/kg). Mice in the budesonide group were exposed to aerosolized budesonide. Pulmonary functions were measured to evaluate the resistance of expiration. The sections were stained with either hematoxylin & eosin to assess the inflammatory cell infiltrates. The levels of interleukin IL-4 and IL-13 in bronchoalveolar lavage fluid (BALF) and total immunoglobulin E (IgE) levels in serum were measured by ELISA. The protein expression of NF-κB in lung tissues was determined by Western blotting assay. Results: Airway inflammation and airway hyperresponsiveness (AHR) were increased in the asthma group. Chrysin significantly inhibited the airway inflammation and AHR, and decreased the levels of IL-4 and IL-13 in BLAF and total IgE levels in serum. In addition, chrysin significantly attenuated the increased protein expression of NF-κB in lung tissues of asthmatic mice. Conclusion: This study demonstrated that chrysin could suppress the progression of airway inflammation and AHR in a murine model of asthma. The effect may be due to inhibition of NF-κB expression.