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タイトル: Oral glucosylceramide reduces 2,4-dinitrofluorobenzene induced inflammatory response in mice by reducing TNF-alpha levels and leukocyte infiltration.
著者: Duan, Jingjing
Sugawara, Tatsuya  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-1203-5521 (unconfirmed)
Sakai, Shota
Aida, Kazuhiko
Hirata, Takashi
著者名の別形: 菅原, 達也
キーワード: Sphingolipids
Dietary supplements
Glucosylceramide
Anti-inflammatory agents
DNFB
BALB/c mice
TNF-α
Immune response
発行日: Jun-2011
出版者: Springer, Part of Springer Science+Business Media
誌名: Lipids
巻: 46
号: 6
開始ページ: 505
終了ページ: 512
抄録: Sphingolipids are constituents of cellular membranes and play important roles as second messengers mediating cell functions. As significant components in foods, sphingolipids have been proven to be critical for human health. Moreover, diverse metabolic intermediates of sphingolipids are known to play key roles both in proinflammatory and in anti-inflammatory effects. However, the effect of dietary sphingolipids on inflammation is a complicated field that needs to be further assessed. Our study evaluated the effects of orally administered maize glucosylceramide (GluCer), one of the most conventional dietary sphingolipids, on inflammation using the 2, 4-dinitro-1-fluorobenzene-treated BALB/c murine model. Oral administration of GluCer inhibited ear swelling and leukocyte infiltration to the inflammatory site, suggesting that dietary GluCer has anti-inflammatory properties. ELISA analyses revealed that oral administration of GluCer for 6 days had not modified the Th1/Th2 balance, but significantly down-regulated the activation of TNF-α at the inflammatory site. Based on these results, the down-regulation of TNF-α by dietary GluCer may suppress vascular permeability and reduce the migration of inflammatory cells. Our findings increase understanding of the actions of dietary sphingolipids on the balance of the immune response.
著作権等: The final publication is available at www.springerlink.com
This is not the published version. Please cite only the published version.
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
URI: http://hdl.handle.net/2433/141847
DOI(出版社版): 10.1007/s11745-010-3518-9
PubMed ID: 21222241
出現コレクション:学術雑誌掲載論文等

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