Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells

BackgroundMethyl lucidone (ML), a methyl derivative of lucidone, has anti-inflammatory properties. However, the molecular mechanisms that reduce inflammatory effect ML in human lung epithelial cells remain unkown. This study aimed to elucidate underlying ML.MethodsFour compounds (ML, linderone, kanakugiol, and linderone) from Lindera erythrocarpa Makino were evaluated for their ability MUC5AC secretion levels phorbol-12-myristate-13-acetate (PMA)-stimulated NCI–H292 using ELISA. The expression response-related proteins analyzed quantitative reverse transcription-PCR, ELISA, western blotting. To determine whether directly regulates TGF-β-activated kinase 1 (TAK1), we performed an vitro assay.ResultsML treatment effectively reduced cytokines, including interleukin-1β TNF-α, increased by stimulation. Furthermore, downregulated pathway cascade both IκB (IKK)/NF-κB p38 MAP kinase/CREB inhibiting upstream TAK1. An analysis confirmed significantly activity TAK1.ConclusionML pretreatment repressed PMA-stimulated inflammation reaction reducing TAK1-mediated IKK/NF-κB mitogen-activated protein (MAP) signaling. These findings suggest may improve respiratory health can be used as dietary supplement or functional food prevent diseases.