| Project/Area Number |
18H02899
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 55050:Anesthesiology-related
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Amaya Fumimasa 京都府立医科大学, 医学(系)研究科(研究院), 教授 (60347466)
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| Co-Investigator(Kenkyū-buntansha) |
佐和 貞治 京都府立医科大学, 医学(系)研究科(研究院), 教授 (10206013)
中川 貴之 京都大学, 医学研究科, 准教授 (30303845)
大橋 憲太郎 岐阜大学, 工学部, 准教授 (50332953)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2020: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2019: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2018: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
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| Keywords | ミトコンドリア / 痛覚過敏 / 慢性痛 |
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| Outline of Final Research Achievements |
Diabetic neuropathy and peripheral nerve injury models were created to evaluate mitochondrial function in primary sensory nerves and to examine the relationship between mitochondrial function and the development of pain hypersensitivity.
In both models, expression of mitochondrial DNA and mitochondrial respiratory chain component proteins in primary sensory neuron was decreased, and mitochondrial membrane potential was reduced, indicating mitochondrial dysfunction. The expression of Parkin, which maintains mitochondrial function, was decreased, and the expression of p53, an inhibitor of Parkin, was increased. p53 inhibitor treatment improved mitochondrial function and attenuated the hyperalgesia observed in the animal models.
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| Academic Significance and Societal Importance of the Research Achievements |
慢性疼痛は難治性であり、あらたな治療法の探索が必要である。本研究において、知覚神経におけるp53の増加がParkinの働きを阻害し、ミトコンドリア機能を低下させること、ミトコンドリア機能の変調が慢性疼痛発症の鍵になることが示された。本研究の成果によって、ミトコンドリア機能改善薬が慢性疼痛治療薬として利用できる可能性が示された。
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