Clarifying the regulatory mechanism of insulin signal in septicemia

  • 横尾, 宏毅 (Principal Investigator)
  • 服部, 裕一 (Co-Investigator(Kenkyū-buntansha))
  • 山本, 誠士 (Co-Investigator(Kenkyū-buntansha))

Project Details

Abstract

We analyzed the insulin signal in septicemia, using the brain and lung tissue in septic model mice. Until the certain period, insulin signal was increased by some defensive mechanisms. However, the signal was reduced gradually, and the degree of tissue damage was increased. Meanwhile, treatment the drugs which maintain the signal reduced the tissue damage. It was expected that the damage in septicemia would be reduced, if we use the protective system via insulin signal, which reduce the oxidative and nitrative stress.
StatusFinished
Effective start/end date2009/01/012011/12/31

Funding

  • Japan Society for the Promotion of Science: ¥4,550,000.00

Keywords

  • 炎症
  • 免疫
  • 敗血症
  • 酸化ストレス
  • ニトロ化ストレス
  • Akt
  • インスリン作用不全
  • NADPH oxidase活性
  • ラジカルスカベンジャー
  • 細胞委縮変形像
  • インスリンシグナル
  • PI3K-Akt
  • 細胞濃染色像
  • 細胞萎縮変形像
  • リモデリング
  • スタチン
  • 核濃染色
  • 核委縮