Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 최한곤 | - |
dc.date.accessioned | 2018-09-06T05:29:24Z | - |
dc.date.available | 2018-09-06T05:29:24Z | - |
dc.date.issued | 2009-04 | - |
dc.identifier.citation | ARCHIVES OF PHARMACAL RESEARCH, v. 32, No. 4, Page. 593-603 | en_US |
dc.identifier.issn | 0253-6269 | - |
dc.identifier.uri | https://link.springer.com/article/10.1007/s12272-009-1416-6 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/74956 | - |
dc.description.abstract | Cell adhesion molecules play a pivotal role in chronic inflammation and pathological angiogenesis. In the present study, we investigated the inhibitory effects of clotrimazole (CLT) on tumor necrosis factor (TNF)-alpha-induced changes in adhesion molecule expression. CLT dose-dependently inhibited monocyte chemoattractant protein-1 (MCP-1), intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expressions in TNF-alpha-stimulated HT29 colonic epithelial cells. This inhibitory action of CLT correlated with a significant reduction in TNF-alpha-induced adhesion of monocytes to HT29 cells, which was comparable to the inhibitory effects of anti-ICAM-1 and VCAM-1 monoclonal antibodies on monocyte-epithelial adhesion. These inhibitory actions of CLT were, at least in part, attributable to the inhibition of redox sensitive NF-kappa B activation, as CLT inhibited TNF-alpha-induced ROS generation as well as NF-kappa B nuclear translocation and activation in HT29 cells. Furthermore, the inhibition of TNF-alpha-induced monocyte adhesion was also mimicked by the specific NF-kappa B inhibitor, pyrrolidine dithiocarbamate (PDTC). Inflammatory mediators including TNF-alpha have known to promote angiogenesis, which in turn further contributes to inflammatory pathology. Therefore, we additionally evaluated whether CLT modulates TNF-alpha-induced angiogenesis using in vivo chick chorioallantoic membrane (CAM) assay. The CAM assay showed that CLT dose-dependently attenuated TNF-alpha-induced angiogenesis, and the effect was correlated with decreased inflammation of the CAM tissue. In conclusion, our results suggest that CLT can inhibit TNF-alpha-triggered expression of adhesion molecules, ICAM-1 and VCAM-1, and angiogenesis during inflammation. | en_US |
dc.description.sponsorship | This research was supported by the Yeungnam University research grants in 2008 (to Jung-Ae Kim). We thank Prati Bajracharya, School of Biotechnology, Yeungnam University for her technical support in immunocytochemistry, and Samil Pharmaceutical Co. Ltd. (Ansan, Korea) and United Pharm. Inc. (Seoul, Korea) for providing CLT. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | PHARMACEUTICAL SOCIETY KOREA | en_US |
dc.subject | Clotrimazole | en_US |
dc.subject | Monocyte adhesion | en_US |
dc.subject | ICAM-1 | en_US |
dc.subject | VCAM-1 | en_US |
dc.subject | NF-kappa B | en_US |
dc.subject | Angiogenesis | en_US |
dc.title | Inhibitory effects of clotrimazole on TNF-alpha-induced adhesion molecule expression and angiogenesis | en_US |
dc.type | Article | en_US |
dc.relation.volume | 32 | - |
dc.identifier.doi | 10.1007/s12272-009-1416-6 | - |
dc.relation.page | 593-603 | - |
dc.relation.journal | ARCHIVES OF PHARMACAL RESEARCH | - |
dc.contributor.googleauthor | Thapa, Dinesh | - |
dc.contributor.googleauthor | Lee, Jong Suk | - |
dc.contributor.googleauthor | Park, Min-A | - |
dc.contributor.googleauthor | Cho, Mi-Yeon | - |
dc.contributor.googleauthor | Park, Young-Joon | - |
dc.contributor.googleauthor | Choi, Han Gon | - |
dc.contributor.googleauthor | Jeong, Tae Cheon | - |
dc.contributor.googleauthor | Kim, Jung-Ae | - |
dc.relation.code | 2009200969 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF PHARMACY[E] | - |
dc.sector.department | DEPARTMENT OF PHARMACY | - |
dc.identifier.pid | hangon | - |
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