| Project/Area Number |
26460629
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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 pharmacology
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| Research Institution | Kumamoto University |
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Principal Investigator |
Ishitsuka Yoichi 熊本大学, 大学院生命科学研究部(薬), 准教授 (70423655)
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| Co-Investigator(Kenkyū-buntansha) |
江良 択実 熊本大学, 発生医学研究所, 教授 (00273706)
竹尾 透 熊本大学, 生命資源研究・支援センター, 講師 (10517014)
中潟 直己 熊本大学, 生命資源研究・支援センター, 教授 (30159058)
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| Co-Investigator(Renkei-kenkyūsha) |
IRIE Tetsumi 熊本大学, 生命科学研究部, 教授 (60150546)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 薬剤性肝障害 / アセトアミノフェン / NPC1 / 医薬品有害反応 / Niemann pick typec / ニーマンピック病C型 / 肝障害 / niemann pick type c |
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| Outline of Final Research Achievements |
This study was conducted to evaluate the roles of Npc1 gene in the development of acetaminophen (APAP)-induced liver injury in mice. We observed that Npc1 null mice were protected from hepatotoxicity induced by APAP overdose compared with wild-type mice. Although significant difference was mot observed in CYP2E1 expression and toxic metabolite production in liver, the key mediators in APAP hepatotoxicity, such as JNK phosphorylation, nitrotyrosine formation and DNA fragmentation were significantly attenuated in Npc1 null mice.
These results suggest that Npc1, at least in part, play a important role in the development of APAP-induced liver injury.
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