| Project/Area Number |
22591973
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
OKU Hidehiro 大阪医科大学, 医学部, 准教授 (90177163)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAI Shinji 大阪医科大学, 医学部, 准教授 (80288703)
FUKUHARA Masayuki 大阪医科大学, 医学部, 非常勤講師 (00238510)
OKUNO Takashi 大阪医科大学, 医学部, 非常勤講師 (20411366)
ISHIZAKI Eisuke 大阪医科大学, 医学部, 助教 (70530434)
KOBAYASHI Takatoshi 大阪医科大学, 医学部, 助教 (10567093)
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| Co-Investigator(Renkei-kenkyūsha) |
HARA Hideaki 岐阜薬科大学, 薬学部, 教授 (20381717)
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| Research Collaborator |
SUGIYAMA Tetsuya 大阪医科大学, 医学部, 講師 (20298764)
HORIE Taeko 大阪医科大学, 医学部, 研究助手
TONARI Masahiro 大阪医科大学, 医学部, 大学院生
MORISHITA Seita 大阪医科大学, 医学部, 大学院生
KURIMOTO Takuji 大阪医科大学, 医学部, 助教 (50388815)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | スタチン / アストロサイト / CD68 / 視神経挫滅モデル / 網膜神経節細胞 / NFκ B / simvastatin / neuro-inflammation / NFκB / NF-κB / TNF-α / iNOS / endothelin / GFAP / 活性化グリア細胞 / 一酸化窒素 / endothelin-1 / real time-PCR |
|---|
| Research Abstract |
We determined neuroprotective properties of systemic statin using optic nerve crush model of rats. There was an accumulation of CD68-positive cells at the crushed site, and the immunoreactivity to MCP-1 was intensified around the lesion. There was an increase in the mRNA levels of the CD68, MCP-1, TNF-α, etc. Systemic statin significantly depressed these inflammatory changes, and rescued the retinal ganglion cells (RGCs) after the injury. Statin significantly reduced the NF-κB activation in cultured astrocytes. Thus, simvastatin may have protective roles on the RGCs possibly through suppression of astroglial NF-κB activation.
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