| Project/Area Number |
10671353
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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 | Nagoya University |
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Principal Investigator |
MATSUYAMA Yukihiko (1999) Nagoya University, School of Medicine, Research Associate, 医学部, 助手 (20312316)
佐藤 公治 (1998) 名古屋大学, 医学部, 講師 (00273235)
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| Co-Investigator(Kenkyū-buntansha) |
KAMIYA Mitsuhiro School of Medicine, Medical Staff, 医学部, 医員
NAKAYAMA Atsuo School of Medicine, Assitant Professor, 医学部, 講師 (50227964)
松山 幸弘 名古屋大学, 医学部, 助手
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | spinal cord injury / Neurotrophic Factor / NGF / apotosis / iNOS / INOS / spinal cord injury / apotosis of spinal cord |
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| Research Abstract |
To investigate pathphysiologycal mechanisms of posttraumatic impairment in the spinal cord using a weight drop technique. Reverse transcriptase-polymerase chain reaction (RT-PCR) revealed that iNOS mRNA arose at 3 h and packed at 12 h after the injury. Immunohistorical analysis showed that iNOS positive cells invaded into the lesioned area through the perivascular space at 6 h after the injury. The population of these cells peaked at 24 h and declined to disappear at 3 d after the injury. The iNOS positive cells were also stained with ED-2 but not with ED-1 and OX-42, indicating that these cells were macrophages and/or perivascular cells. Paralelled with the appearance of iNOS positive cells, there emerged cells positively stained by the terminal deoxynucleotidy-transferase-mediated dUDP-biotin nick end-labeling (TUNEL) assay. The TUNEL positive cells scattered in the lesional area at 1 d after the injury, however, some uprose nearby the iNOS positive cells.
Administration of L-Ng-nitro-arginine methylester (L-NAME), a competitive inhibitor of NOS, resulted in the reduction of TUNEL positive cells in the lesioned area. These results suggested that nitric oxide (NO) through iNOS of macrophages and/or perivascular cells plays an important role in eliminating damaged cells via apoptosis from the lesioned area.
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