A study of neurogenic bone lesion in neuropathic pain model (2);using immobilized model mouse and osteopetrosis mouse
Project/Area Number |
15591632
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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 |
Anesthesiology/Resuscitation studies
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Research Institution | HIROSHIMA UNIVERSITY |
Principal Investigator |
KAWAGUCHI Kotaro Hiroshima University, Graduate School of Health Sciences, Assistant Professor, 大学院・保健学研究科, 助教授 (60263703)
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Co-Investigator(Kenkyū-buntansha) |
YUGE Osafumi Hiroshima University, Graduate School of Biomedical Science, Professor, 医歯薬総合研究科, 教授 (40034128)
TUTUMI Eriko Hiroshima University, Graduate School of Health Sciences, Assistant, 大学院・保健学研究科, 助手 (40304422)
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Project Period (FY) |
2003 – 2005
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Project Status |
Completed (Fiscal Year 2005)
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Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2004: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2003: ¥2,600,000 (Direct Cost: ¥2,600,000)
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Keywords | CCI model / immobilized model / bone atrophy / neuropathic pain / macrophage / TNF-α |
Research Abstract |
Neuropathic pain has many uncertain points of the cause. In addition, neuropathic pain is sometimes accompanied by bone atrophy. We examined bone atrophy by using enzymeimmunochemistry. Additionally, we also examined the relationships between macrophages, tumor necrosis factor (TNF)-α and thermal hyperalgesia by using behavioristy, biochemistry and immunohistochemistry. In former examination, we made neuropathic pain (CCI), immobilized (IMO) and immobilized with neuropathic pain model (IC). Then, we stained osteoclasts and substance P (SP) by TRAP staining and immunohistochemistry, respectively. Then, we calculated osteoclasts number per area. In latter examination, we made neuropahtic pain model to normal mouse (control) and osteopetrosis (op/op) mouse, whose macrophages are absent congenitally. Then, we measured withdrawal thresholds time, analyzed TNF-α by western blotting, and observed macrophages and TNF-α by immunohistochemistry. Osteoclasts number was larger in ipsilateral side than in contralateral side in CCI and IC at post-1 week, and in IC at post-3 weeks. However, they were not significantly differences between three groups. In SP immunoreactivity, deep staining areas were observed in CCI and IC, but there were not significantly different between these groups. In latter examination, at post-12 hours, thermal hyperalgesia was observed in control but not op/op, and expression of macrophages and TNF-α was fewer in op/op than in control. At post-5 days, thermal hyperalgesia was observed in both, but expression of macrophages and TNF-α was similar in post 12 hours. Upregulation of osteoclasts in CCI may be occurred by some factors other than immobilization. There are possibilities that macrophages and TNF-α may relate to thermal hyperalgesia at early phase after nerve lesion, but may not relate to thermal hyperalgesia as time passed. It is necessary to research relations between bone atrophy and neuropeptides other than SP, and change of central nervous system.
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Report
(4 results)
Research Products
(3 results)