| Project/Area Number |
24592737
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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 |
Emergency medicine
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| Research Institution | Yamaguchi University |
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Principal Investigator |
FUJITA Motoki 山口大学, 医学(系)研究科(研究院), 助教 (50380001)
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| Co-Investigator(Kenkyū-buntansha) |
TSURUTA Ryosuke 山口大学, 大学院医学系研究科, 教授 (30263768)
ODA Yasutaka 山口大学, 大学院医学系研究科, 准教授 (40397998)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 頭部外傷 / HMGB1 / ニューロン / オリゴデンドロサイト / 軸索損傷 / 壊死 / 脳挫傷 |
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| Outline of Final Research Achievements |
In this study, HMGB1 translocated from the nucleus to the cytoplasm in neurons and oligodendrocytes as early as 10 min post injury and such cytoplasmic HMGB1 was associated with necrosis in the early phases of lateral fluid percussion injury (LFPI). Therefore, cytoplasmic HMGB1 expression might be a potential marker of necrosis in the acute phases of traumatic brain injury (TBI). In addition, necrotic changes in oligodendrocytes were associated with the onset diffuse axonal injury-mediated Wallerian degeneration in the corpus callosum because these necrotic changes in oligodendrocytes accompanied local axonal damage. Further, hypothermia therapy which suppressed superoxide generation and HMGB1 suppression therapy with glycyrrhizin (GL) or recombinant human thrombomodulin (rhTM) revealed protective effects against axonal injury after LFPI. These findings indicated that HMGB1 might be one of the therapeutic target of TBI and that these therapies might be novel therapies of TBI.
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