Inhibitory Effects of Protopanaxadiol on Lipopolysaccharide-Induced Reactive Oxygen Species Production and MUC5AC Expression in Human Airway Epithelial Cells

Abstract

Background and Objectives MUC5AC is one of the major secretory mucin genes in the human airway epithelium. MUC5AC expression is increased by a variety of inflammatory mediators. Protopanaxadiol (PPD), one of the major active metabolites in ginseng, is known to have anti-inflammatory, antitumor and antioxidant properties. However, the effects of PPD on mucin secretion of airway epithelial cells still have not been reported. Therefore, the aim of this study is to investigate the effect of PPD on lipopolysaccharide (LPS)-induced MUC5AC expression in human airway epithelial cells. Materials and Method In the mucin-producing human NCI-H292 airway epithelial cells, the effect of PPD on MUC5AC expression was investigated using reverse transcription-polymerase chain reaction and enzyme immunoassay after treated with LPS. N-acetylcysteine (NAC) as a reactive oxygen species (ROS) scavenger, and apocynin as a nicotinamide adenine dinucleotide phosphate oxidase inhibitor were used to compare the inhibitory effect of PPD on LPSinduced ROS production in human NCI-H292 cells. Results LPS significantly increased MUC5AC mRNA expression and protein production. LPS also increased ROS production. PPD inhibited LPS-induced MUC5AC mRNA expression and protein production as well as ROS production. In addition, NAC and apocynin inhibited LPS-induced MUC5AC mRNA expression and protein production. Conclusion These results demonstrate that PPD inhibits LPS-induced MUC5AC expression via ROS in human airway epithelial cells and the inhibitory effect of PPD was similar to that of NAC and apocynin. These findings indicate that PPD may be a therapeutic agent for control of mucus secretion and oxidative stress in human airway epithelial cells. Key words: Human airway epithelial cells ㆍ MUC5AC ㆍ Protopanaxadiol ㆍ Reactive oxygen species