| Project/Area Number |
22659326
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Emergency medicine
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| Research Institution | Chiba University |
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Principal Investigator |
WATANABE Eizo 千葉大学, 大学院・医学研究院, 講師 (40375639)
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| Co-Investigator(Kenkyū-buntansha) |
ODA Shigeto 千葉大学, 大学院・医学研究院, 教授 (90204205)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,340,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | オートファジー / 敗血症 / 細胞死 / 腹膜炎 / 盲腸結紮穿孔 / 集中治療 |
|---|
| Research Abstract |
It is not well understood whether the process of autophagy is accelerated or blocked, and whether it is beneficial or harmful to the immune defense mechanism over a time course during sepsis. Our aim was to determine both the kinetics and the role of autophagy in sepsis. We examined autophagosome and autolysosome formation in a cecal ligation and puncture (CLP) mouse model of sepsis (in C57BL/6N mice and GFP-LC3 transgenic mice), using western blotting, immunofluorescence, and electron microscopy. All autophagy-related processes are activated in a mouse model of early sepsis. Also, inhibition of autophagy process by chloroquine administration immediately after CLP resulted in liver injury and higher mortality; autophagy appears to play a protective role in septic animals.
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