| Project/Area Number |
18591989
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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 |
Emergency medicine
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| Research Institution | Showa University |
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Principal Investigator |
DOHI Kenji Showa University, School of Medicine, Associate professor (20301509)
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| Co-Investigator(Kenkyū-buntansha) |
ARUGA Toru Showa University, School of Medicine, Professor (40266086)
SHIODA Seiji Showa University, School of Medicine, Professor (80102375)
YOFU Sachiko Showa University, School of Medicine, Researcher (00398695)
SATOH Kazue Showa University, School of Medicine, Professor (90053941)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,690,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | free radical / neurotrauma / oxidative stress / animal model / mice / knockout / gp91phox / NADPH / 神経科学 / 頭部外傷 / ラット / ESR / gp91 |
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| Research Abstract |
(Introduction)
The sources of superoxide radical (O2-) production following traumatic brain injury (TBI) are known as some cascades: cyclooxygenase, xanthine oxygenase, NADPH oxygenase. In this study, the kinetics and the roles of gp9lphox(gp91) after traumatic brain injury were investigated using gp9lphox gene knockout mouse.
(Material and Methods)
C57BL mice were used in this study. In the current study, we investigated the time-dependent changes in the expression of the gp9lphox in the mice traumatic brain injury model (TBI) (controlled cortical impact model) using western blotting method. The gp91 positive cells were identified by double immunohistochemical technique. The damaged areas of wild mouse and gp9lphox knockout mouse were also measured on day2 after TBI. Superoxide radical levels were detected by in situ detection of oxidized Het.
(Results)
On day 2 after TBI, the gp91 phox was strongly expressed in microglia mainly. The damaged area was suppressed in gp91 phox knockout mouse. Production of superoxide radical was also suppressed in gp91 phox knockout mouse.
These results indicate that gp91phox and NADPH has the important roles as a generator of free radical in TBI.
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