Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 배정호 | * |
dc.date.accessioned | 2016-08-29T11:08:47Z | - |
dc.date.available | 2016-08-29T11:08:47Z | - |
dc.date.issued | 2009 | * |
dc.identifier.issn | 1945-8924 | * |
dc.identifier.other | OAK-5822 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/232028 | - |
dc.description.abstract | 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)-1beta-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-1beta 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-1beta -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. Copyright © 2009, OceanSide Publications, Inc., U.S.A. | * |
dc.language | English | * |
dc.title | [6]-Gingerol suppresses interleukin-1β-induced MUC5AC gene expression in human airway epithelial cells | * |
dc.type | Article | * |
dc.relation.issue | 4 | * |
dc.relation.volume | 23 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 385 | * |
dc.relation.lastpage | 391 | * |
dc.relation.journaltitle | American Journal of Rhinology and Allergy | * |
dc.identifier.doi | 10.2500/ajra.2009.23.3337 | * |
dc.identifier.wosid | WOS:000268797300004 | * |
dc.identifier.scopusid | 2-s2.0-70349249938 | * |
dc.author.google | Kim J.H. | * |
dc.author.google | Chang J.H. | * |
dc.author.google | Yoon J.-H. | * |
dc.author.google | Kwon S.H. | * |
dc.author.google | Bae J.H. | * |
dc.author.google | Kim K.-S. | * |
dc.contributor.scopusid | 배정호(35168533900;57199910352) | * |
dc.date.modifydate | 20231120162154 | * |