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dc.contributor.author김정애ko
dc.contributor.author박수민ko
dc.contributor.author수실렉미ko
dc.contributor.author박수영ko
dc.contributor.author이은경ko
dc.contributor.author장재훈ko
dc.contributor.author구세광[구세광]ko
dc.contributor.author김동희[김동희]ko
dc.date.accessioned2015-12-17T04:08:54Z-
dc.date.available2015-12-17T04:08:54Z-
dc.date.created2015-11-13-
dc.date.issued201407-
dc.identifier.citationEUROPEAN JOURNAL OF PHARMACOLOGY, v.735, pp.184 - 192-
dc.identifier.issn0014-2999-
dc.identifier.urihttp://hdl.handle.net/YU.REPOSITORY/31472-
dc.identifier.urihttp://dx.doi.org/10.1016/j.ejphar.2014.04.024-
dc.description.abstractPro-inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, are pivotal for the development of inflammatory bowel disease (IBD), and down-regulation of the cytokines and cytokine-induced inflammatory responses therefore constitute pharmacological targets for the development of therapeutic strategies in IBD. In the current study, we found that 7-O-succinyl macrolactin A (SMA), a macrolide, potently inhibited TNF-alpha-induced adhesion of monocytes to colonic epithelial cells in a concentration-dependent manner, similar to rapamycin, a mTOR inhibitor. In addition, oral administration of SMA resulted in a significant suppression of clinical signs of TNBS-induced rat colitis, including weight loss, colon tissue edema, and myeloperoxidase activity, a marker for inflammatory cell infiltration, as well as microscopic damage score in a histomorphological examination of HE-stained colon tissue. More importantly, SMA was more efficacious in inhibition of intestinal inflammation than 5-aminosalicylic acid (5-ASA), an active metabolite of sulfasalazine, the most commonly prescribed agent for the treatment of IBD. Such anti-inflammatory activity showed correlation with significant suppression of adhesion molecules (ICAM-1 and VCAM-1), T-helper 1-type cytokines (TNF-alpha, IL-6), and chemokines (MCP-1, IL-8). In addition to inhibition of NF-kappa B nuclear translocation, SMA also caused significant suppression of TNF-alpha-induced phosphorylation of PI3K, Akt, mTOR and p70S6 kinase, similar to the effect of rapamycin, an immunosuppressant macrolide. Taken together, the current results suggest that managing both mTOR and NF-kappa B activation pathways using SMA may be a good therapeutic intervention for the treatment of IBD. (C) 2014 Elsevier B.V. All rights reserved.-
dc.language영어-
dc.publisherELSEVIER SCIENCE BV-
dc.subjectTUMOR-NECROSIS-FACTOR-
dc.subjectINTERCELLULAR-ADHESION MOLECULE-1-
dc.subjectVANCOMYCIN-RESISTANT ENTEROCOCCI-
dc.subjectSULFATE-INDUCED COLITIS-
dc.subjectBOWEL-DISEASE-
dc.subjectCROHNS-DISEASE-
dc.subjectULCERATIVE-COLITIS-
dc.subjectTNF-ALPHA-
dc.subjectSTAPHYLOCOCCUS-AUREUS-
dc.subjectT-CELLS-
dc.titleProtective effect of 7-O-succinyl macrolactin A against intestinal inflammation is mediated through PI3-kinase/Akt/mTOR and NF-kappa B signaling pathways-
dc.typeArticle-
dc.identifier.wosid000338599300022-
dc.identifier.scopusid2-s2.0-84899774975-
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