| Project/Area Number |
20590095
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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 |
Biological pharmacy
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| Research Institution | Yokohama College of Pharmacy |
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Principal Investigator |
TOMOBE Koji Yokohama College of Pharmacy, 薬学部, 講師 (80460286)
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| Co-Investigator(Kenkyū-buntansha) |
NOMURA Yasuyuki 横浜薬科大学, 薬学部, 教授 (00034041)
KANEKO Masayuki 千葉科学大学, 薬学部, 講師 (10322827)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 老化 / 老化促進マウス / 酸化ストレス / 老化促進マウ / 小胞体ストレス / 蛋白質 |
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| Research Abstract |
In this study, we investigated the mechanism underling the development of accelerated senescence in SAMP8 mice. Oxidative stress is a cause of aging, and is systemically accumulated in SAMP8. Thus, we estimated Nrf2, oxidative stress sensor, in the liver of SAMP8 and SAMR1 by Western Blot analysis. The protein level of Nrf2 in the nucleus of the liver was significantly decreased in SAMP8. In addition, the phosphorylation of Akt and GSK-3b was significantly decreased in the liver of SAMP8. Thus, it is suggested that the reduction of the translocation of Nrf2 into the nucleus might be induced by a decrease of GSK-3b phosphorylation, resulting in an increase of oxidative stress in SAMP8 mice.
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