| Project/Area Number |
07671520
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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 |
Cerebral neurosurgery
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
KAWAUCHI Masamitsu OKAYAMA UNIVERSITY MEDICAL SCHOOL ASSISTANT, 医学部, 助手 (20252950)
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| Co-Investigator(Kenkyū-buntansha) |
TOMITA Susumu OKAYAMA UNIVERSITY MEDICAL SCHOOL ASSISTANT, 医学部, 助手 (90237115)
後藤 正樹 岡山大学, 医学部・附属病院, 医員
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | head injury / oxigen radical / SOD / ESR / hypothermia / SEP |
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| Research Abstract |
Oxygen-derived free radicals have been reported to be involved in the secondary self-destructive mechanisms occuring after TBI.
In the present study, we investigated the intensity of brain hydroxyl radical (OH) generation, using electoron spin trapping method (ESR), and lipidperoxidation to examine the relationship between free radicals and lipid peroxidative tissue damage. And we analyzed endogenous Cu, Zn-SODmRNA expression and SOD activity to examine the effect of lecithinized SOD (PC-SOD) on TBI.
Our results show that the degree of posttraumatic brain edema as closely correlated with the increase of the generation of OH radical and lipid peroxidation tissue damage. PC-SOD increased SOD activity and decreased brain edema.
These findings demonstrate that superoxide may play an important role in development of edema after TBI,and suggest the potential the rapeutic selectiviey of the PC-SOD therapy strategy.
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