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The Expression Pattern of Pro- and Antiapoptotic Proteins Bax and Bcl-2 in Rat Brain Neurons in Response to Severe Hypobaric Hypoxia: The Correcting Effect of Hypoxic Preconditioning

机译:严重低压缺氧对大鼠脑神经元促凋亡和抗凋亡蛋白Bax和Bcl-2表达的影响:低氧预处理的纠正作用

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摘要

In the early 1980s, the phenomenon of delayed neu-ronal death several days after ischemia was described in hippocampal neurons [1]. It was then demonstrated that the neuronal injury observed developed by the apop-totic mechanism (programmed cell death) with an involvement of genes and killer proteins. This neuronal death caused by severe forms of ischemia/hypoxia has been reported in susceptible brain areas other than hippocampus: neocortex, striatum, and cerebellum [2-4].
机译:在1980年代初期,海马神经元描述了缺血后几天神经元延迟死亡的现象[1]。然后证明了观察到的神经元损伤是由凋亡机制(程序性细胞死亡)发展而来,涉及基因和杀伤蛋白。据报道,由严重的局部缺血/缺氧引起的这种神经元死亡发生在海马以外的易感大脑区域:新皮层,纹状体和小脑[2-4]。

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