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Inhibition of MUC5AC gene expression by anethole in human airway epithelial cell via TAK1-MAPK-AP-1 and TAK1-IκB-NF-κB pathways
DC Field | Value | Language |
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dc.contributor.author | 이은정 | - |
dc.date.accessioned | 2017-07-11T16:10:27Z | - |
dc.date.available | 2017-07-11T16:10:27Z | - |
dc.date.issued | 2016 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/149186 | - |
dc.description | Dept. of Medicine/박사 | - |
dc.description.abstract | Mucin overproduction is a hallmark of chronic rhinosinusitis. Natural compounds with mucin-suppressive property are attractive and effective as mucin regulatory agents in airway diseases such as chronic rhinosinusitis. The aim of this study was to investigate whether anethole suppresses interleukin (IL)-1β induced MUC5AC gene expression in human airway epithelial cells and whether this activity of anethole is related to TAK1-MAPK-AP-1 and TAK1-IκB-NF-κB signaling pathways. NCI-H292 cells were pretreated with 50 μM of anethole for 1 h, then 10 ng/mL of IL-1β was added for 24 h. MUC5AC mRNA expression was then measured by real-time PCR. The phosphorylation levels of proteins were assayed by western blot. The nuclear components of NF-κB and AP-1 were assayed using luciferase activity. And the nuclear translocation of NF-κB and AP-1 from cytosol was observed by the confocal laser scanning microscopy. Cell survival remained above 90% in the presence of anethole at a concentration of 50 μM. IL-1β induced MUC5AC mRNA expression was significantly decreased by 50 μM anethole, to the level of the untreated control group, as opposed to an increase to 3.2 ± 0.5-fold for IL-1β alone, and this suppression of MUC5AC expression was dose-dependent. This decrease in MUC5AC expression by anethole was mediated via the MAPK pathway, such as phospho-p38 and phospho-ERK. And the suppression of MUC5AC by anethole was also mediated via the TAK1-MAPK-AP-1 and TAK1-IκB-NF-κB signaling pathways. In suppressing IL-1β-induced MUC5AC gene expression by anethole, NF-κB or AP-1 was important transcription factor. These results suggest that anethole suppresses IL-1β-induced MUC5AC gene expression in human airway epithelial cells via the TAK1-MAPK-AP-1 and TAK1-IκB-NF-κB signaling pathways, and may be considered an anti-hypersecretory agent. | - |
dc.description.statementOfResponsibility | open | - |
dc.publisher | Graduate School, Yonsei University | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Inhibition of MUC5AC gene expression by anethole in human airway epithelial cell via TAK1-MAPK-AP-1 and TAK1-IκB-NF-κB pathways | - |
dc.title.alternative | 사람 호흡기 상피세포에서 TAK1-MAPK-AP-1과 TAK1-IκB-NFκB 경로를 통한 anethole의 MUC5AC 유전자 발현 억제 작용 | - |
dc.type | Thesis | - |
dc.contributor.alternativeName | Lee, Eun Jung | - |
dc.type.local | Dissertation | - |
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