Plantamajoside Inhibits Lipopolysaccharide-Induced MUC5AC Expression and Inflammation through Suppressing the PI3K/Akt and NF-kappa B Signaling Pathways in Human Airway Epithelial Cells

It has been reported that plantamajoside (PMS), a major natural compound isolated from Plantago asiatica, has anti-inflammatory activities. However, the effect of PMS on respiratory inflammatory diseases has not yet been studied. The present study aimed to evaluate the effect of PMS on lipopolysaccharide (LPS)-induced airway inflammation and the underlying mechanism. The results showed that PMS did not affect the cell viability of 16-HBE cells. PMS (20 and 40 mu g/ml) decreased the expression levels of MUC5AC, IL-6, and IL-1 beta, which were induced by LPS treatment. PMS inhibited the LPS-induced phosphorylation of Akt and p65. In addition, inhibitors of the PI3K/Akt and NF-kappa B pathways attenuated the effect of LPS on 16-HBE cells. In conclusion, PMS inhibits LPS-induced MUC5AC expression and inflammation through suppressing the PI3K/Akt and NF-kappa B signaling pathways, indicating that PMS may be a potential therapy for the treatment of respiratory inflammatory diseases.