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Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease

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タイトル: Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease
著者: Ichikawa, Nobuki 著作を一覧する
Yamashita, Kenichiro 著作を一覧する
Funakoshi, Tohru 著作を一覧する
Ichihara, Shin 著作を一覧する
Fukai, Moto 著作を一覧する
Ogura, Masaomi 著作を一覧する
Kobayashi, Nozomi 著作を一覧する
Zaitsu, Masaaki 著作を一覧する
Yoshida, Tadashi 著作を一覧する
Shibasaki, Susumu 著作を一覧する
Koshizuka, Yasuyuki 著作を一覧する
Tsunetoshi, Yusuke 著作を一覧する
Sato, Masanori 著作を一覧する
Einama, Takahiro 著作を一覧する
Ozaki, Michitaka 著作を一覧する
Umezawa, Kazuo 著作を一覧する
Suzuki, Tomomi 著作を一覧する
Todo, Satoru 著作を一覧する
キーワード: Inflammatory bowel disease
3-[(Dodecylthiocarbonyl)-methyl]-glutarimide
Trinitrobenzenesulfonic acid
Dextran sulfate sodium
Colitis
Macrophage
発行日: 2016年 3月
出版者: Springer
誌名: Inflammation Research
巻: 65
号: 3
開始ページ: 245
終了ページ: 260
出版社 DOI: 10.1007/s00011-015-0911-0
抄録: Objective and design: To examine the effect of 3-[(dodecylthiocarbonyl)-methyl]-glutarimide (DTCM-G), a novel anti-inflammatory agent that inhibits lipopolysaccharide (LPS) activation of RAW264.7 macrophages, on murine models of colitis and RAW264.7 cells. Materials and methods: Colitis was induced by rectally infusing trinitrobenzenesulfonic acid (TNBS) (1.5 mg in 50 % ethanol) in BALB/c mice or orally administering 3 % dextran sulfate sodium (DSS) for 5 days in C57BL/6 mice. The severity of colitis was assessed after intraperitoneally injecting DTCM-G (40 mg/kg). The anti-inflammatory properties of DTCM-G and its mechanisms were investigated in LPS-stimulated RAW264.7 cells. Results: DTCM-G significantly ameliorated TNBS-induced colitis, according to the body weight loss, disease activity index, colonic obstruction, macroscopic colonic inflammation score, mucosal myeloperoxidase activity, and histopathology. Immunohistochemistry and isolated lamina propria mononuclear cells showed significantly reduced colonic F4/80+ and CD11b+ macrophage infiltration. DTCM-G significantly suppressed tumor necrosis factor (TNF)-α and interleukin (IL)-6 messenger RNA expression in the colon and attenuated DSS-induced colitis, according to the disease activity index and histopathology. In RAW264.7 cells, DTCM-G suppressed LPS-induced TNF-α/IL-6 production and enhanced glycogen synthase kinase-3β phosphorylation. Conclusions: DTCM-G attenuated murine experimental colitis by inhibiting macrophage infiltration and inflammatory cytokine expression. Thus, DTCM-G may be a promising treatment for inflammatory bowel disease.
Rights: The final publication is available at link.springer.com
資料タイプ: article (author version)
URI: http://hdl.handle.net/2115/64632
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 市川 伸樹

 

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