Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 남태규 | - |
dc.date.accessioned | 2023-04-25T04:15:44Z | - |
dc.date.available | 2023-04-25T04:15:44Z | - |
dc.date.issued | 2018-02 | - |
dc.identifier.citation | JOURNAL OF CROHNS & COLITIS, v. 12.0, Page. S142-S143 | - |
dc.identifier.issn | 1873-9946;1876-4479 | - |
dc.identifier.uri | https://academic.oup.com/ecco-jcc/article/12/supplement_1/S142/4807879 | en_US |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/179298 | - |
dc.description.abstract | Background Inflammatory bowel disease (IBD) is characterised by a chronic inflammation of gastrointestinal tract with unknown aetiology. Oxidative stress is one of contributing factors associated with the disease severity of IBD, and currently has been implicated as a therapeutic target. Previous studies showed that BJ-1108, a derivative of 6-amino-2,4,5-trimethylpyridin-3-ol, significantly inhibited reactive oxygen species (ROS) generation resulting in suppression of tumour growth in vitro. We therefore investigated the effects of BJ-1108 on dextran sulfate sodium (DSS)-induced experimental colitis in mice. Methods DSS-induced colitis was made by two cycles of DSS (2%) administration followed by 7-day water administration. The effect of BJ-1108 was also evaluated in vitro using Caco-2 cells. Results DSS-treated mice exhibited severe colitis, whereas mice administrated BJ-1108 improved the disease severity indicated by body weight, histological scores, spleen weight, T cell and macrophage infiltrates. BJ-1108 administration also inhibited colonic expression of NF-kB p65 and IL-1β in vivo. In addition, BJ-1108 treated mice had the enhanced epithelial barrier function indicated by in vivo intestinal permeability and the expression of tight junction proteins such as ZO-1, occludin, claudin-1 and claudin-3 in DSS-induced colitis model. Next, we used in vitro Caco-2 cells to confirm the effects of BJ-1108 on ROS generation and barrier function. As expected, BJ-1108 treated Caco-2 cells significantly ameliorated the cytokine-induced ROS generation in dose-dependent manner. In addition, BJ-1108 remarkably recovered in vitro injured-barrier functions assessed by transepithelial electrical resistance and tight junction protein expression in dose-dependent manner. Finally, we founded that BJ-1108 suppressed NF-kB p65 and PI3K/AKT pathway, and slightly p38/JNK pathway in time-dependent manner. Conclusions Collectively, these results provided that BJ-1108 had a therapeutic potential for IBD through reduction of ROS generation and inhibition of NF-kB and PI3K/AKT pathway. | - |
dc.language | en | - |
dc.publisher | OXFORD UNIV PRESS | - |
dc.title | BJ-1108, a 6-Amino-2,4,5-trimethylpyridin-3-ol analogue, ameliorates DSS-induced colitis in mice | - |
dc.type | Article | - |
dc.relation.volume | 12.0 | - |
dc.identifier.doi | 10.1093/ecco-jcc/jjx180.224 | - |
dc.relation.page | S142-S143 | - |
dc.relation.journal | JOURNAL OF CROHNS & COLITIS | - |
dc.contributor.googleauthor | Cho, H. J. | - |
dc.contributor.googleauthor | Kim, E. S. | - |
dc.contributor.googleauthor | Lee, H. | - |
dc.contributor.googleauthor | Kim, J. -A. | - |
dc.contributor.googleauthor | Jeong, B. -S. | - |
dc.contributor.googleauthor | Nam, T. -g. | - |
dc.contributor.googleauthor | Lee, Y. -J. | - |
dc.sector.campus | E | - |
dc.sector.daehak | 약학대학 | - |
dc.sector.department | 약학과 | - |
dc.identifier.pid | tnam | - |
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