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Investigation concerning the pathogenesis of septic condition, and development of new therapy by PPARγ activation in monocytic cells.

Research Project

Project/Area Number 23792079
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Emergency medicine
Research InstitutionKyoto Prefectural University of Medicine

Principal Investigator

FUKAZAWA Madoka  京都府立医科大学, 医学部附属病院, 専攻医 (30530357)

Project Period (FY) 2011 – 2012
Project Status Completed (Fiscal Year 2012)
Budget Amount *help
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Keywords遺伝子治療 / 敗血症 / RNA干渉法 / 単球系細胞
Research Abstract

We obtained macrophage from healthy volunteers. After the differentiation into macrophage, they were cultured in different glucose concentrations of cell culture liquid for 72 hours after lipopolysaccharide administration. High glucose conditions reduced phagocytic ability and exaggerated cell death in macrophage by the activation of endoplasmic reticulum stress. Ghrelin administration reversed these effects through peroxisome proliferator-activated receptor (PPARγ) activation.

Report

(3 results)
  • 2012 Annual Research Report   Final Research Report ( PDF )
  • 2011 Research-status Report
  • Research Products

    (2 results)

All 2013

All Presentation (2 results)

  • [Presentation] 敗血症病態の高糖環境におけるマクロファージ貪食能低下に寄与する細胞内情報伝達機序と炎症消退脂質による抑制効果2013

    • Author(s)
      石井祥代,中嶋康文,飯田淳,村瀬百子,深澤まどか,佐和貞治
    • Organizer
      日本麻酔科学会第60回学術集会
    • Place of Presentation
      札幌
    • Related Report
      2012 Final Research Report
  • [Presentation] 敗血症病態の高糖環境におけるマクロファージ貪食能低下に寄与する細胞内情報伝達機序と炎症消退脂質による抑制効果2013

    • Author(s)
      石井祥代,中嶋康文,飯田淳,村瀬百子,深澤まどか,佐和貞治
    • Organizer
      日本麻酔科学会学術集会
    • Place of Presentation
      札幌
    • Related Report
      2012 Annual Research Report

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Published: 2011-08-05   Modified: 2019-07-29  

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