2010 Fiscal Year Final Research Report
Oxidative stress-induced apoptotic cell death pathway after spinal cord injury
Project/Area Number |
20591704
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
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Research Institution | Akita University |
Principal Investigator |
SUZUKI Akira Akita University, 大学院・医学系研究科, 助教 (10311573)
|
Co-Investigator(Kenkyū-buntansha) |
SUGAWARA Taku 秋田大学, 医学部, 講師 (80241660)
|
Project Period (FY) |
2008 – 2010
|
Keywords | 脊髄損傷 / 運動ニューロン / アポトーシス / DNA損傷 / スーパーオキシド |
Research Abstract |
Ventral horn motor neurons (VMN) are selectively vulnerable to mild spinal cord injury (SCI) ; however, the mechanisms of cell death had not been understood. Mild compression SCI was induced in Sprague-Dawley rats, and superoxide production and apoptotic DNA injury were characterized. Increased superoxide production was observed exclusively in VMN after SCI. Subsequently, a majority of VMN (80%) selectively underwent delayed apoptotic cell death. These results suggest that the oxidative stress plays a pivotal role in apoptotic VMN death after SCI.
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