Project/Area Number |
15K00844
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Eating habits
|
Research Institution | Juntendo University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
長岡 功 順天堂大学, 医学(系)研究科(研究院), 教授 (60164399)
|
Project Period (FY) |
2015-04-01 – 2019-03-31
|
Project Status |
Completed (Fiscal Year 2018)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | グルコサミン / 抗炎症 / O-GlcNAc修飾 / 炎症性サイトカイン / NF-κB / p65 / 炎症 |
Outline of Final Research Achievements |
Glucosamine (GlcN), a natural amino monosaccharide, is used as a nutritional supplement for ‘joint health’, and anti-inflammatory action of GlcN is involved in its protective action of joint disorder. In this study, we examined the molecular mechanisms of GlcN for exerting the anti-inflammatory action. GlcN inhibited the nuclear-factor of κB (NF-κB), an important transcription factor for the production of inflammatory mediators, and the inhibitor of κB kinase (IKK)β, an upstream regulator of NF-κB. GlcN induced the O-linked-N-acetylglucosamine (O-GlcNAc) modification of NF-κB and IKKβ. O-GlcNAc modification was involved in the regulation of NF-κB and IKKβ functions. From these results, GlcN is inferred to inhibit the expression of inflammatory mediators via the O-GlcNAc modification of NF-κB and IKKβ.
|
Academic Significance and Societal Importance of the Research Achievements |
慢性炎症は老化とともに起こる様々な疾患や、生活習慣病、がんなどの多彩な疾患の基盤病態と考えられている。したがって慢性炎症を制御することが、これら疾患の予防につながる。本研究成果は、炎症抑制効果をもち長期服用可能なグルコサミンがサプリメントとして慢性炎症の予防に有効である可能性を示している。さらに新しい抗炎症薬の開発にO-GlcNAc修飾がターゲットとなりうることを示した点で意義がある研究成果と思われる。
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