| Project/Area Number |
22791752
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Emergency medicine
|
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
|
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| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
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| Keywords | 敗血症 / 高血糖 / 単球系細胞 / 炎症消退脂質 / 炎症性消退脂質 / RNA干渉法 |
|---|
| Research Abstract |
To make a in vitro model of septic condition, monocytic cells were exposed with lipopolysaccaride and hyperglycemia, which induced apoptosis, inhibited secretion of proinflammatory cytokine, and phagocytosis. Our results suggest that ER stress and Akt phosphorylation are primary involved as the upstream modulator. Furthermore, Resolvin D2, known as a lipid mediator in resolution of inflammation, suppressed apoptosis and improved phagocytosis, which results indicate that Resolvin D2 have the potential lipid mediator for treating sepsis.
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