Abstract: Objective: To explore the protective activity of Hawthorn polyphenols (HBPs) against the Benzoapyrene (BaP)-induced Human bronchial epithelial cells (16HBE) inflammatory damages. Methods: The HBPs were isolated in a bio-assay guidedbioassay-guided method. The MTT assay method was used to evaluate the cytotoxicity of HBPs, and the CCK 8 assay method was used to detect the protective activity of HBPs against the BaP-induced 16HBE cells cells inflammatory damages. ELISA was performed to evaluate the levels of inflammatory epithelial cytokines and ROS. Flow cytometry was used to detect the 16HBE cells cells apoptosis. Western blotting was used to detect the effect of HBP-1 onproteins on the proteins expression of NF-κB and AhR signals. Results: Ten HBPs were isolated, and the structure of HBPs were identified. In the currecurrentnt experiment, the HBP-1[(Z)-1-(2,4-dihydroxy-6-methoxy-3-(3-methylbut-1-en-1-yl)-5-(3-methylbut-2-en-1-yl) phenyl) ethan-1-one] performed the most protective activity against BaP-induced cell viability decline. HBP-1 inhibited BaP-induced inflammatory epithelial cytokines (TNF-α, IL-1β and IL-18) over-release and inhibited the intracellular ROS up-regulation. HBP-1 suppressed the BaP-induced 16HBE cells apoptosis. HBP-1 also inhibited the BaP-induced AhR and NF-κB signals activation. Conclusion: HBP-1 inhibits the BaP-induced inflammatory damages and cell apoptosisby apoptosis by inhibiting the inflammatory epithelial cytokines over-release and the AhR and NF-κB signals activation.

Key words: Hawthorn, Benzoapyrene, Polyphenol, AhR, NF-κB