| Project/Area Number |
15591592
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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 |
Orthopaedic surgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
YONE Kazunori Kagoshima University, Graduate School of Medical and Dental Sciences, Associate Professor, 大学院・医歯学総合研究科, 助教授 (40182844)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAMINE Tomonori Kagoshima University, University Hospital, Faculty of Medicine and Dentistry, Research Associate, 医学部・歯学部附属病院, 助手 (10359979)
YOKOUCHI Masahiro Kagoshima University, Graduate School of Medical and Dental Sciences, Research Associate, 大学院・医歯学総合研究科, 助手 (80359976)
KOMIYA Setsuro Kagoshima University, Graduate School of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (30178371)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2004: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | spinal cord injury / apoptosis / erythropoietin / spinal cord degeneration / 脊髄損傷 |
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| Research Abstract |
In the present study, we evaluated antiapoptotic effects of EPO in both cerebrocortical culture and an animal model of acute spinal cord injury. In vitro study employing cerebrocortical culture demonstrated preventative effect of erythropoietin on N-methyl-D-aspartate-induced neuronal apoptosis. Spinal cord injury was produced in rats by applying extradural static weight-compression at T-9 level. These injured rats received either EPO(5000 units/kg) or an equal volume of physiological saline solution by intraperitoneal injection 15 minutes and 24 hours after injury. These rats were killed between 6 hours and 7 days after injury, and specimens obtained were examined histologically and subjected to immunostaining by monoclonal antibody against active caspase3 and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL). There was a significant difference between untreated rats and EPO-treated rats in the number of TUNEL-positive cells between 6 hours and 7 days after injury. The percentages of cells expressing active caspase3 was significantly lower in EPO-treated rats than in untreated rats 3 days after injury. Destructive spinal cord changes, including cavity formation and demyelination, were less apparent in EPO-treated rats. These findings suggest that exogenous EPO reduces apoptosis and results in inhibition of destructive spinal cord changes following traumatic injury.
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