| Project/Area Number |
24500871
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Applied health science
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| Research Institution | Nippon Medical School |
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Principal Investigator |
YOKOTA TAKASHI 日本医科大学, 付置研究所, その他 (30445829)
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| Co-Investigator(Kenkyū-buntansha) |
OHTA Shigeo 日本医科大学, 大学院医学研究科, 教授 (00125832)
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| Co-Investigator(Renkei-kenkyūsha) |
WOLF Alexsander 日本医科大学, 先端医学研究所細胞生物学部門, 講師 (20434136)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 水素分子 / 酸化ストレス / 抗酸化 / 水素 / 緑内障 / 抗酸化剤 |
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| Outline of Final Research Achievements |
Oxidative and nitrative processes have an important role in the pathogenesis of glaucomatous neurodegeneration. Ｅxposure of a nitric oxide donor, S-nitroso-N-acetylpenicillamine (SNAP) induce neuronal damage independently of peroxynitrite. We cultured rat retinal tissues in an organotypic culture system with SNAP, in the presence or absence of Molecular hydrogen (H2). H2 suppressed loss of mitochondrial membrane potential and apoptosis in retinal cells. Moreover, H2 decreased the tyrosine nitration level and suppressed oxidative stress damage in retinal cells. SNAP treatment decreased the cell numbers in the retinal cell layer, but the presence of H2 inhibited this reduction. These findings suggest that H2 has a neuroprotective effect against retinal cell oxidative damage, presumably by scavenging peroxynitrite.
Thus, H2 may be an effective and novel clinical tool for treating glaucoma and other oxidative stress-related diseases.
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