Abstract: Objective　To investigate the effect of naringenin on airway inflammation in asthmatic rats and its mechanism. Methods　The rat model of asthma was induced with ovalbumin. Rats were divided into normal control group, OVA model group, naringenin 100 mg/kg group and naringenin 200 mg/kg group. After finishing the experiment, the asthmatic rats were anesthetized and sacrificed. Giemsa staining was used to detect the number and classification of inflammatory cells in bronchoalveolar lavage fluid (BALF). HE staining was used to observe pathological changes in lung tissue. ELISA was used to detect the content of NF-κB in serum and the Th2 cytokines in BALF. The NF-κB protein and mRNA expression levels in asthmatic rats were detected by immunohistochemistry and qPCR. Lipopolysaccharide (LPS) was used to induce A549 inflammatory cell model. The expression of NF-κB protein in A549 cells after naringenin treatment was detected by immunofluorescence and Western blot assay. Results　Both the naringenin 100 mg/kg and naringenin 200     mg/kg can reduce the infiltration of monocytes, neutrophils, eosinophils and lymphocytes on lungs and bronchus in asthmatic rats, and can improve the physiological structure of alveoli, reduce bronchial mucosal epithelium shedding, promote bronchial pseudostratification and ciliary structure repairment. Naringenin can reduce the expression levels of NF-κB p65, NF-κB p50 protein and mRNA in lungs (P＜0.05). The serum contents of NF-κB p65 and NF-κB p50 and the Th2 cytokines IL-4, IL-5, IL-13 in BALF were significantly decreased after treatment with naringenin (P＜0.05). In in vitro LPS-induced inflammatory A549 cells, naringenin could reduce the expression levels of NF-κB p65 and NF-κB p50 proteins, and reverse the expression of IκBα (P＜0.05). Conclusion　Naringenin can effectively reduce the inflammatory response in lungs and bronchus of asthmatic rats, and its potential mechanism is related to the inhibition of NF-κB signaling pathway.