Project/Area Number |
26750362
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Biomolecular chemistry
|
Research Institution | Tokyo University of Agriculture and Technology |
Principal Investigator |
Suzuki Eriko 東京農工大学, (連合)農学研究科(研究院), 助教 (00468513)
|
Research Collaborator |
Hasumi Keiji 東京農工大学, 大学院農学研究院, 教授 (20208474)
|
Project Period (FY) |
2014-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | 抗炎症 / IL-6 / 生理活性物質 / SMTP / 可溶性エポキシドハイドロラーゼ / 脂質代謝 / 炎症 / エネルギー代謝 / 脂質代謝改善 |
Outline of Final Research Achievements |
Our DNA microarray data derived from SMTP-treated mice and sEH KO mice, there was a strinking similarity regarding the gene expression patten. Those includes Lcn2 and Saa, which are all upregulated under IL-6 signaling. We therefore focused on sympathetic nerve system leading to IL-6 signaling, determined whether AR activation enhances SMTP-mediated IL-6 secretion in vivo. As a result, SMTP-induced IL-6 secretion was synergistically enhanced by alpha and beta AR agonist. Interestingly, only beta2 AR antagonist effectively inhibited SMTP-induced IL-6 secretion, suggesting that beta2 AR downstream signaling is involved in SMTP/sEH inhibition-mediated anti-inflammatory action in vivo.
|
Academic Significance and Societal Importance of the Research Achievements |
本研究課題において遂行した、微生物由来生理活性物質SMTPによる抗炎症活性の機序解明が、現在脳梗塞治療薬として臨床開発段階にあるSMTP同族体の薬効を説明する上で非常に重要な意義を持つことは明らかであり、今後、より詳細な分子機序に迫るための展望が見出せた。
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