Effect of Platycodin D on Airway MUC5AC Mucin Production and Gene Expression Induced by Growth Factor and Proinflammatory Factor

Abstract

Abstract － In this study, we tried to investigate whether platycodin D significantly affects MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF), phorbol ester (PMA) and tumor necrosis factor-α (TNF-α) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of platycodin D for 30 min and then stimulated with EGF, PMA and TNF-α for 24h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) Platycodin D was found to inhibit the production of MUC5AC mucin protein induced by EGF, PMA, and TNF-α, respectively. (2) It also inhibited the expression of MUC5AC mucin gene induced by the same inducers. These results suggest that platycodin D can regulate mucin gene expression and production of mucin protein, by directly acting on human airway epithelial cells. Keywords: Airway mucin, MUC5AC, Platycodin D INTRODUCTION Airway mucus is very important in defensive action against invading pathogenic microorganisms, chemicals and particles. This defensive action of airway mucus is at-tributed to the physicochemical property of mucins i.e. viscoelasticity. Mucins are multimillion dalton glycoproteins present in the airway mucus and produced by goblet cells in the surface epithelium as well as mucous cells in the submucosal gland. However, hypersecretion of airway mu-cus is one of the major symptoms associated with severe pulmonary diseases including asthma, chronic bronchitis, cystic fibrosis and bronchiectasis (Ellis, 1985). Therefore, we suggest it is valuable to find the potential activity of reg-ulating (inhibiting) the excess mucin secretion (production) by the compounds derived from various medicinal plants. We have tried to investigate the possible activities of some natural products on mucin secretion from cultured airway epithelial cells. As a result of our trial, we previously re-ported that several natural compounds affected mucin se-cretion and/or production from airway epithelial cells (Lee