Casticin alleviates lipopolysaccharide-induced inflammatory responses and expression of mucus and extracellular matrix in human airway epithelial cells through Nrf2/Keap1 and NF-κB pathways.

Asthma is one of the most common chronic inflammatory diseases of childhood, characterized by airway inflammation, mucus hypersecretion, and accumulation of extracellular matrix proteins. Casticin is an active compound that possesses broad biological activities including anti-inflammatory effect. However, the effect of casticin on asthma remains unknown. The aim of the present study was to evaluate the effect and mechanism of casticin on inflammatory responses and expression of mucus and extracellular matrix in human airway epithelial cells. The results showed that lipopolysaccharide induced the mRNA and protein levels of IL-6, IL-8, MUC5AC, collagen type I, and fibronectin in 16-HBE cells, whereas casticin treatment significantly inhibited the induction of lipopolysaccharide. Casticin induced Nrf2/Keap1 and inhibited nuclear factor κB pathways in 16-HBE cells. Knockdown of Nrf2 attenuated the effect of casticin on production of IL-6 and IL-8, expression of MUC5AC, collagen type I, and fibronectin in 16-HBE cells. In conclusion, the results indicated that casticin might be a novel therapeutic strategy for the treatment of asthma.