Objective:To study the effect of galangin on ozone exposure-induced airway inflammation of chronic obstructive pulmonary disease (COPD) in mice and to explore its possible mechanism. Methods:A total of 32 male C57BL/6 mice were randomly divided into four classes:the control group,COPD group,COPD+galangin group and galangin group. They were exposed to ozone for 3 h per day,twice a week for a period of 12 weeks. The control mice were exposed to normal air. Lung sections were stained with hematoxylin-eosin (HE) to assess inflammatory cell infiltration. Bronchoalveolar lavage fluid (BALF) was collected to detect cell counts and cytokines level by enzyme linked immunosorbent test (ELISA). Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to assess the expression of nuclear factor-erythroid related factor 2 (Nrf-2) mRNA and Kelch-like ECH-associated protein1 (Keap1) mRNA. Results:Airway inflammatory cell infiltration in the COPD group significantly increased,and inflammatory cells,interleukin (IL-) 6,IL-8 and TNF-α in the BALF were also notably increased in the COPD group compared with the control group (P < 0.05). Galangin significantly alleviated the severity of airway inflammation and inhibited IL-6,IL-8 and TNF-α secretion (P < 0.05). At the same time,galangin significantly increased Nrf-2 mRNA expression,while Keap1 mRNA had no significant change. Conclusion:Galangin can effectively inhibit the occurrence and progression of COPD airway inflammation,possibly due to the Nrf2-keap1 antioxidant system.