Stress Response in Cerebral Ischemia and the Role of Ubiquitin

脑缺血是最常见的脑代谢应激之一。短暂的局部缺血不会杀死神经元，它会引发应激反应。一旦应激蛋白被诱导，神经元获得对进一步缺血的短暂耐受。泛素就是这样一种应激蛋白。然而，在CA 1锥体细胞中，游离泛素在缺血后迟发性神经元死亡之前就已耗尽。我们的实验已经通过免疫染色、免疫印迹、免疫沉淀和免疫吸收试验证明了这一点。通过ELISA定量，我们还显示了缺血后CA 1神经元中游离形式的ubiq的耗尽和伴随的缀合泛素的增加。原位杂交方法采用与沙土鼠泛素基因互补的c-DNA，缺血后泛素基因表达增强。这种短暂的转录增加而翻译减少也见于缺血后的热休克蛋白70基因。CA 1区神经元迟发性死亡的机制尚不清楚。虽然泛素在神经元死亡中的实际作用还不清楚，但对泛素基因表达的进一步研究可能揭示海马Ca 1神经元中这种形式的神经元的机制。

Cerebral ischemia is one of the most frequent metabolic stress to the brain. A brief period of ischemia does not kill neurons and it triggers stress response. Once stress proteins are induced, neurons acquire transient tolerance to further ischemia. Ubiquitin is one of such stress proteins. In CA1 pyramidal cells, however, free ubiquitin is depleted far before delayd neuronal death following ischemia. Our experiment has shown this by immunostaining, immunoblotting, immunoprecipitation, and immunoabsorption assays. By ELISA quantitation, we also have shown the depletion of free form of ubiq and concomitant increase in conjugated ubiquitin in CA1 neurons following ischemia. In-situ hybridization method using c-DNA complimentary to gerbil ubiquitin gene, gene expression for ubiquitin is rather enhanced following ischemia. This transient increase in transcription yet decrease in translation is also seen in hsp 70 gene following ischemia. The mechanism of delayd neuronal death of CA1 neurons is still unknown. Although the actual role of ubiquitin in neuronal death is also not known, further investigation of ubiquitin gene expression might reveal the mechanism of this form of neuronal in hippocampal Ca1 neurons.