[不同低压缺氧模式下神经元转录因子NF-kappaB的表达规律]。

M. Samoilov, A. Churilova, T. Glushchenko, K. Baranova
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引用次数: 2

摘要

转录因子NF-kappaB在损伤性刺激下,首先是不同类型的缺氧,脑神经元的存活和退化机制中起着关键作用。在本研究中,我们使用定量免疫化学方法,分析了NF-kappaB不同亚基(p65和c-Rel)在大鼠新皮层中对严重损伤性低压缺氧(HH)或单次或多次轻度保护性缺氧(HH)的反应。严重缺氧(SH)导致脑神经元的损失,对p65的表达水平没有影响,但抑制c-Rel的表达。多次(但不是一次)使用轻度HH进行预处理的试验可以减少神经元损伤,促进p65的表达,并防止SH后c-Rel水平的抑制。三次使用轻度HH作为预处理刺激时,可上调这两个亚单位的表达,而单次或六次试验对这两个亚单位的免疫反应性水平没有影响。p65和c-Rcl表达的特性表明,NF-kappaB的这些亚基似乎与脑对SH的耐受机制有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Pattern of neuronal expression of transcription factors NF-kappaB under different modes of hypobaric hypoxia].
Transcription factor NF-kappaB plays a pivotal role in mechanisms of brain neuron survival and degeneration under injurious stimuli, first of all different types of hypoxia. In the present work, using quantitative immunohystochemistry, we provide analysis of expression of different subunits of NF-kappaB (p65 and c-Rel) in the rat neocortex in response to severe injurious hypobaric hypoxia (HH) or after a single or multiple sessions of mild protective HH. Severe hypoxia (SH), resulting in loss of brain neurons, has no effect on the level of expression of p65 but suppresses expression of c-Rel. Multiple (but not single one) trials of preconditioning using mild HH which reduce neuronal damage promote p65 expression and prevent suppression of c-Rel level after SH. Triple session of mild HH itself when applied as a preconditioning stimulus upregulate expression of both subunits, while single administration or sixfold trials has no effect on the level of immunoreactivity of both subunits. The revealed peculiarities of the expression of p65 and c-Rcl implies that these subunits of NF-kappaB appear to contribute to the mechanisms of brain tolerance to SH.
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