| Project/Area Number |
15K10306
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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 |
Neurosurgery
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| Research Institution | Fukuoka University (2016-2017)
The University of Tokushima (2015) |
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Principal Investigator |
Yagi Kenji 福岡大学, 医学部, 講師 (80551837)
|
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| Co-Investigator(Kenkyū-buntansha) |
宇都 義浩 徳島大学, 大学院社会産業理工学研究部(生物資源産業学域), 教授 (20304553)
永廣 信治 徳島大学, 病院, 病院長 (60145315)
|
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 脳・神経 / 脳梗塞 / Ｍ１/Ｍ２様マクロファージ / 炎症性サイトカイン / phagocytosis / 神経再生 / Ｍ１/Ｍ２マクロファージ / 炎症性ｻｲﾄｶｲﾝ |
|---|
| Outline of Final Research Achievements |
Brain ischemia promotes the recruitment of various cell types to the brain. Group-specific component protein-derived macrophage activating factor (GcMAF) has various functions including activation of M2-type macrophages and the improvement of motor disability. We tested whether activation of M2-type macrophage by GcMAF after brain ischemia induces beneficial effects. In the early phase of post-ischemia, GcMAF had no beneficial effects. In the late phase, it promoted the clearance of the infarct area; elevated the mRNA level of arginase-1 and increased CD163+ M2-like macrophages in the peri-infarct region. They co-localized with CD36+- and CD68+- but not Iba-1+ cells.. Treatment with GcMAF increased in the incorporation of BrdU and the appearance of NeuN+ and MAP2+ cells in the peri-infarct region mildly improved the neurological deficit. The activation of M2-like macrophages by GcMAF in the late phase may play a therapeutic role.
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