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Heat shock protein 72 production and the protection effect for the cardiac fibroblast cells in response to cold shock treatment.

机译:热休克蛋白72的产生以及对冷休克治疗后心脏成纤维细胞的保护作用。

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摘要

Expression of heat shock proteins has been induced by several stimuli, e.g., hypoxia, ischemia, heat shock and drugs. It is not known whether cold shock induces heat shock stress proteins in the heart. The author employed isolated cultured cardiac cells to test the hypothesis that cold shock is a type of stress that induces heat shock proteins. Cultured cells from a rat heart were subjected to 30, 60 and 120 minutes of cold shock at 4 degrees Celsius followed by re-warming up to 37 degrees Celsius and incubated for 24 hours. Cells were isolated and expression of heat shock protein 72 was determined by Western blots. Results demonstrated significant expression of heat shock protein 72 in cold-shocked cells. This expression was dependent on the duration of the normothennic recovery after cold shock and showed the effect of protection from anoxic and re-oxygenation insult. These observations demonstrated that cold shock was cardioprotective following cold preservation and cardioplegic arrest. Heat shock protein induction played a role in this protection.
机译:热休克蛋白的表达已经由几种刺激诱导,例如缺氧,局部缺血,热休克和药物。尚不清楚冷休克是否会在心脏中诱发热休克应激蛋白。作者采用离体培养的心脏细胞来检验以下假设:冷休克是一种诱导热休克蛋白的应激。将来自大鼠心脏的培养细胞在4摄氏度下进行30、60和120分钟的冷休克,然后重新加热至37摄氏度,并孵育24小时。分离细胞并通过蛋白质印迹法测定热休克蛋白72的表达。结果表明,冷休克细胞中热休克蛋白72大量表达。该表达取决于冷休克后降冰片恢复的持续时间,并显示出对缺氧和复氧损伤的保护作用。这些观察结果表明,冷保存和心脏停搏后,冷休克具有心脏保护作用。热激蛋白的诱导在这种保护中起作用。

著录项

  • 作者

    Gao, Shiping.;

  • 作者单位

    Southern Connecticut State University.;

  • 授予单位 Southern Connecticut State University.;
  • 学科 Biophysics Medical.;Biology Molecular.;Biology Cell.
  • 学位 M.S.
  • 年度 2002
  • 页码 41 p.
  • 总页数 41
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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