| Project/Area Number |
25350634
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | Teikyo University of Science & Technology |
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Principal Investigator |
HAGIWARA HIROKI 帝京科学大学, 公私立大学の部局等, 教授 (80276732)
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| Co-Investigator(Kenkyū-buntansha) |
Masaki Toshihiro 帝京科学大学, 医療科学部, 教授 (00585028)
SAITO Fumiaki 帝京大学, 医学部, 准教授 (40286993)
HIROSE Noboru 帝京科学大学, 医療科学部, 准教授 (60460391)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | レスベラトロール / サーチュイン 1 / 先天性筋ジストロフィー / 筋原性制御因子 / 線維化 / オステオポンチン / 廃用性筋萎縮 / 筋萎縮筋原性制御因子 / 筋萎縮 / 酸化ストレス / 糖脂質代謝 |
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| Outline of Final Research Achievements |
Resveratrol (RSV), a naturally derived polyphenol, has recently shown to exhibit anti-aging effects by activating SIRT1 (sirtuin 1). To examine the long-term therapeutic potential of on muscular dystrophies, we examined whether pathogenesis in dy-2J mice (a model for congenital muscular dystrophy type 1A (MDC1A)) is ameliorated by prolonged administration of resveratrol. RSV was orally administered ad libitum to mice for over 1 year. We compared resveratrol administrated (RSV-treated) with control (non-treated) groups by physiological and histological analyses. RSV-treated group showed a significant improve in body weight, muscle strength and locomotive activities than control group. By histological analysis, we found that RSV-treated group showed larger in cell size and less fibrosis in comparison with control group. These results suggest that long-term administration of resveratrol suppresses the progression of muscular dystrophy in dy-2J model mice by reducing fibrosis.
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