| Project/Area Number |
15K08025
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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 |
Drug development chemistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
Ozawa Koichiro 広島大学, 医歯薬保健学研究科(薬), 教授 (10211822)
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| Co-Investigator(Kenkyū-buntansha) |
杉山 政則 広島大学, 医歯薬保健学研究科(薬), 共同研究講座教授 (30106801)
細井 徹 広島大学, 医歯薬保健学研究科(薬), 准教授 (40379889)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ALDH / 小胞体ストレス / アルデヒドデヒドロゲナーゼ / フルルビプロフェン |
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| Outline of Final Research Achievements |
We previously found that flurbiprofen, one of the nonsteroidal anti-inflammatory drugs, can ameliorate endoplasmic reticulum stress (ER stress). Furthermore, we previously found that flurbiprofen may interact with aldehyde dehydrogenase (ALDH). In the present study, by using recombinant ALDH protein, we found that flurbiprofen can induce activation of ALDH activity. Additionally, we found possibility that ALDH may form aggregate in the mitochondria by ER stress-inducing reagent and this aggregation was reduced by flurbiprofen. These results suggest that flurbiprofen may increase ALDH activity and attenuate ER stress-induced aggregation of ALDH.
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