| Project/Area Number |
26462244
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
SAKUMA Eisuke 名古屋市立大学, 大学院医学研究科, 講師 (90295585)
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| Co-Investigator(Kenkyū-buntansha) |
和田 郁雄 名古屋市立大学, 大学院医学研究科, 教授 (70182970)
若林 健二郎 名古屋市立大学, 大学院医学研究科, 助教 (20418867)
伊藤 錦哉 名古屋市立大学, 大学院医学研究科, 研究員 (50597820)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 再生医療 / ミクログリア / 下垂体前葉 / 脊髄損傷 / 炎症 / 下垂体 / 移植 / 濾胞星細胞 / ギャップジャンクション / レプチン / ズッカーラット |
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| Outline of Final Research Achievements |
In the acute spinal injury, we must try to minimize the inflammation of the spinal cord tissue. We try to rescue this inflammation and investigate the mechanism to suppress the microglia for minimizing the inflammation. The ghrelin system activated by Rikkunshito significantly reduced the number of pathologically activated microglia with amoeboid morphology in the brains of klotho-deficient, SAMP8 and aged ICR mice. We also report that SGK1 and SGK3 are expressed in multiple microglial cell lines. An SGK inhibitor, gsk650394, inhibits cell viability. In addition, lipopolysaccharide-induced expression of inflammatory regulators iNOS and TNFa was enhanced by gsk650394. These findings suggest that SGKs may play an important role in regulating microglial viability and inflammatory responses. These two investigations include the important findings to rescue this inflammation of the spinal cord tissue.
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