| Project/Area Number |
24790639
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Legal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
UNUMA Kana 東京医科歯科大学, 医歯(薬)学総合研究科, 講師 (30586425)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | autophagy / endotoxemia / heme oxygenase-1 / lipopolysaccharide / 肝臓 / 敗血症 / オートファジー / カルバモイルリン酸シンターゼ1 / 一酸化炭素 / CPS1 |
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| Research Abstract |
A large reduction in liver mitochondrial protein and induction of autophagy were observed in LPS-treated rats.Electron microscopic and immunohistochemical analyses demonstrated autophagic vacuoles in LPS-treated rat liver. Oxidative stress markers were increased in LPS-treated animals; CoPP treatment ablated these alterations. An inhibitor for the opening of mitochondrial permeability transition pore, cyclosporine A, suppressed oxidative stress as well as liver damage during LPS administration. CoPP promoted auto- phagy and prevented rats from liver damage during LPS administration.HO-1 promotes autophagy and elimination of damaged mitochondria thereby repressing oxidative stress in LPS-treated rat liver, revealing a novel mechanism for protec- tion by HO-1 against septic liver damage.
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