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大鼠脑短暂性缺血后干扰素调节因子-1 mRNA 水平的变化。

Changes in interferon-regulatory factor-1 mRNA levels after transient ischemia in rat brain.

作者信息

Paschen W, Gissel C, Althausen S, Doutheil J

机构信息

Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Köln, Germany.

出版信息

Neuroreport. 1998 Oct 5;9(14):3147-51. doi: 10.1097/00001756-199810050-00005.

Abstract

To evaluate whether the interferon system in the brain is activated by a severe form of metabolic stress, and to elucidate the possible mechanism underlying this activation, changes in the interferon regulatory factor-1 (irf-1) mRNA levels were evaluated after transient cerebral ischemia, and after exposure of primary neuronal cells to experimental conditions resulting in a depletion of ER calcium stores. Following 30 min ischemia and 2 h recovery, irf-1 mRNA levels rose significantly and stayed high for up to 24 h of recovery. Irf-1 mRNA levels were also significantly increased in neurons in vitro after exposing cells to conditions resulting in ER calcium store depletion with or without a parallel increase in cytoplasmic calcium activity. It is concluded that transient cerebral ischemia induces activation of the interferon system and that disturbances of ER calcium homeostasis may play a role in this process.

摘要

为评估大脑中的干扰素系统是否会被严重形式的代谢应激激活,并阐明这种激活背后的可能机制,研究人员在短暂性脑缺血后,以及将原代神经元细胞暴露于导致内质网钙储存耗竭的实验条件下后,评估了干扰素调节因子-1(irf-1)mRNA水平的变化。在缺血30分钟并恢复2小时后,irf-1 mRNA水平显著上升,并在恢复长达24小时内保持高位。在将细胞暴露于导致内质网钙储存耗竭的条件下后,无论细胞质钙活性是否同时增加,体外培养的神经元中irf-1 mRNA水平也显著升高。得出的结论是,短暂性脑缺血会诱导干扰素系统的激活,内质网钙稳态的紊乱可能在此过程中起作用。

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