Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 김정목 | - |
dc.date.accessioned | 2018-03-27T00:26:11Z | - |
dc.date.available | 2018-03-27T00:26:11Z | - |
dc.date.issued | 2012-09 | - |
dc.identifier.citation | IMMUNOLOGY, 2012, 137(1), P.98-113 | en_US |
dc.identifier.issn | 0019-2805 | - |
dc.identifier.issn | 1365-2567 | - |
dc.identifier.uri | https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2567.2012.03618.x | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/52792 | - |
dc.description.abstract | 5,7-Dih ydroxy-3′,4′,6′-trimethoxyflavone (eupatilin), the active pharmaco-logical ingredient from Artemisia asiatica Nakai (Asteraceae), is reportedto have a variety of anti-inflammatory properties in intestinal epithelialcells. However, little information is known about the molecular mechanismof eupatilin-induced attenuation of bronchial epithelial inflammation. Thisstudy investigates the role of eupatilin in the adhesion of inflammatorycells such as monocytes and eosinophils to bronchial epithelial cells. Stim-ulation of a human bronchial epithelial cell line (BEAS-2B) with tumournecrosis factor-a (TNF-a) increased the expression of surface adhesionmolecules, including intercellular adhesion molecule 1 (ICAM-1) and vas-cular cell adhesion molecule 1 (VCAM-1), in which eupatilin significantlyinhibited the expression of those adhesion molecules in a dose-dependentmanner. Eupatilin suppressed the TN F- a -induced activation of IjBa andnuclear factor-jB (NF-jB) signals in BEAS-2B cells. The IjB kinase (IKK)activation was also significantly reduced in eupatilin-pre-trea ted BEAS-2Band primary normal human bronchial epithelial (NHB E) cells. However,eupatilin did not influence AP-1 activity in TNF-a-stimulated cells.Suppression of NF-jB signalling induced by eupatilin resulted in the inhi-bition of the exp ression of adhesion molecules and the adhesion of mono-cytes and eosinophils to BEAS-2B cells. Furthermore, eupatilin suppressedthe phosphorylation of Akt in TNF-a-stimulated BEAS-2B and NHBE cells,leading to down-regulation of NF-jB activation and adhesion moleculeexpression and finally to suppression of the inflammatory cell adhesi on toepithelial cells. These results suggest that eupatili n can inhibit the adhesionof inflammatory cells to bronchial epithelial cells via a signalling pathway,including activation of Akt and NF-jB, as well as expression of adhesionmolecules | en_US |
dc.description.sponsorship | This research wassupported by Basic Science Research Program throughthe National Research Foundation of Korea (NRF)funded by the Ministry of Education, Science and Tech-nology (MEST) (No. 2010-0008594) and a grant from theNRF of Korea Grant funded by the Korean Government(MEST) (MRC Program No. 2010-0029507) | en_US |
dc.language.iso | en | en_US |
dc.publisher | Wiley | en_US |
dc.subject | adhesion | en_US |
dc.subject | eupatilin | en_US |
dc.subject | intercellular adhesion molecule | en_US |
dc.subject | nuclearfactor-jB | en_US |
dc.subject | vascular cell adhesion molecule | en_US |
dc.title | 5,7-dihydroxy-3,4,6-trimethoxyflavone inhibits intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 via the Akt and NF-κB-dependent pathway, leading to suppression of adhesion of monocytes and eosinophils to bronchial epithelial cells. | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 137 | - |
dc.identifier.doi | 10.1111/j.1365-2567.2012.03618.x | - |
dc.relation.page | 98-113 | - |
dc.relation.journal | IMMUNOLOGY | - |
dc.contributor.googleauthor | Jung, Jireh | - |
dc.contributor.googleauthor | Ko, Su H | - |
dc.contributor.googleauthor | Yoo, Do Y | - |
dc.contributor.googleauthor | Lee, Jin Y | - |
dc.contributor.googleauthor | Kim, Yeong-Jeon | - |
dc.contributor.googleauthor | Choi, Seul M | - |
dc.contributor.googleauthor | Kang, Kyung K | - |
dc.contributor.googleauthor | Yoon, Ho J | - |
dc.contributor.googleauthor | Kim, Hyeyoung | - |
dc.contributor.googleauthor | Kim, Jung M | - |
dc.relation.code | 2012211890 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jungmogg | - |
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