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Objective: To investigate the effects of casticin (CAS) on lipopolysaccharide-induced injury of human normal lung epithelial cells (BEAS-2B) and NF-κB-Keap1-Nrf2/ARE pathway. Methods: BEAS-2B cells were pretreated with different concentrations of casticin for 1 h, 2 h and 4 h, and then treated with 1 µg/ml liposolysaccharide to construct cell damage model. The contents of inflammatory factors in cell supernatant was detected by ELISA to screen the optimal concentration and time of casticin. The cells were divided into normal group, model group, Casticin group, ML385 group, Casticin+ML385 group and dexamethasone group. Cell apoptosis was detected by flow cytometry, the concentrations of inflammatory factors were detected by ELISA, and the levels of NF-κB p65, p-NF-κB p65, Keapl, Nrf2 and Nrf2 protein in cell nucleus were detected by Western blot. Results: The optimal concentration of CAS was 10 µmol/L and the optimal time was 2 h. Compared with normal group, the apoptosis rate, the contents of inflammatory factors, p-NF-κB p65 and Keap1 protein expression levels in model group were significantly increased (P<0.01), and Nrf2 protein expression levels in cells and nuclei were significantly decreased (P<0.01). Compared with model group, apoptosis rate and contents of inflammatory factors in casticin group and dexamethasone group were significantly decreased (P<0.01), protein expression levels of p-NF-κB p65 and Keap1 in Casticin group were significantly decreased (P<0.01). The expression level of Nrf2 protein in cells and nuclei was significantly increased (P<0.01). Compared with ML385 group, apoptosis rate, inflammatory factors contents, p-NF-κB p65 and Keap1 protein expression levels in Casticin+ML385 group were significantly decreased (P<0.01), the expression level of Nrf2 protein in cells and nuclei were significantly increased (P<0.01). Conclusion: CAS can inhibit cell inflammation induced by lipo-polysaccharide by regulating NF-κB-Keap1-Nrf2/ARE signaling pathway. [ABSTRACT FROM AUTHOR]