BACKGROUND: [6]-Gingerol is a major active component of ginger and a natural polyphenol compound. The present study investigated whether [6]-gingerol suppresses interleukin (IL)-1 beta-induced MUC5AC gene expression in human airway epithelial cells and, if so, examined whether the suppression of MUC5AC gene expression is mediated via the mitogen-activated protein kinase (MAPK) signal transduction pathway. METHODS: MUC5AC mRNA and protein were measured using reverse transcription-polymerase chain reaction (PCR), real-time PCR, and Western blot analysis in cultured NCI-H292 human airway epithelial cells. Extracellular signal-regulated kinase (ERK) and p38 MAPK protein levels were analyzed by Western blot. RESULTS: Expression of MUC5AC mRNA increased in NCI-H292 cells upon treatment with 10 ng/mL of IL-1 beta for 24 hours. When the cells were pretreated with 10 microM of [6]-gingerol, expression of IL-1 beta-induced MUC5AC mRNA and protein was significantly suppressed. Suppression of IL-1 beta-induced MUC5AC mRNA was also observed in cells pretreated with ERK- or p38 MAPK-specific inhibitors, suggesting that [6]-gingerol-mediated suppression of IL-1 beta-induced MUC5AC mRNA operated via the ERK- and p38 MAPK-dependent pathways. CONCLUSIONS: [6]-Gingerol suppresses IL-1 beta -induced MUC5AC gene expression in human airway epithelial cells via the ERK- and p38 MAPK-dependent pathways; therefore, [6]-gingerol may be considered a possible anti-hypersecretory agent.
BACKGROUND:[6]-Gingerol is a major active component of ginger and a natural polyphenol compound. The present study investigated whether [6]-gingerol suppresses interleukin (IL)-1 beta-induced MUC5AC gene expression in human airway epithelial cells and, if so, examined whether the suppression of MUC5AC gene expression is mediated via the mitogen-activated protein kinase (MAPK) signal transduction pathway. METHODS:MUC5AC mRNA and protein were measured using reverse transcription-polymerase chain reaction (PCR), real-time PCR, and Western blot analysis in cultured NCI-H292 human airway epithelial cells. Extracellular signal-regulated kinase (ERK) and p38 MAPK protein levels were analyzed by Western blot. RESULTS: Expression of MUC5AC mRNA increased in NCI-H292 cells upon treatment with 10 ng/mL of IL-1 beta for 24 hours. When the cells were pretreated with 10 microM of [6]-gingerol, expression of IL-1 beta-induced MUC5AC mRNA and protein was significantly suppressed. Suppression of IL-1 beta-induced MUC5AC mRNA was also observed in cells pretreated with ERK- or p38 MAPK-specific inhibitors, suggesting that [6]-gingerol-mediated suppression of IL-1 beta-induced MUC5AC mRNA operated via the ERK- and p38 MAPK-dependent pathways. CONCLUSIONS:[6]-Gingerol suppresses IL-1 beta -induced MUC5AC gene expression in human airway epithelial cells via the ERK- and p38 MAPK-dependent pathways; therefore, [6]-gingerol may be considered a possible anti-hypersecretory agent.