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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Hypoxic preconditioning induces neuroprotection against transient global ischemia in adult rats via preserving the activity of Na(+)/K(+)-ATPase.
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Hypoxic preconditioning induces neuroprotection against transient global ischemia in adult rats via preserving the activity of Na(+)/K(+)-ATPase.

机译：缺氧预处理通过保留Na（+）/ K（+）-ATPase的活性诱导成年大鼠对短暂性全局缺血的神经保护作用。

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摘要

We demonstrated previously that 30min of hypoxic preconditioning (HPC) applied 1day before 10min of transient global cerebral ischemia (tGCI) reduced neuronal loss in the hippocampal CA1 subregion in adult rats. The aim of the present study was to investigate the role of Na(+)/K(+)-ATPase and protein kinase Mzeta (PKMzeta) in the protective effect of HPC against tGCI in adult rats. We found that the activity of Na(+)/K(+)-ATPase decreased in the hippocampal CA1 subregion after 10min of tGCI. This effect was not seen after 30min of HPC in adult rats. Corresponding to the changes in Na(+)/K(+)-ATPase activity, the surface expression of Na(+)/K(+)-ATPase alpha1 subunit increased after HPC. Furthermore, HPC dramatically reduced the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells in the hippocampal CA1 subregion after tGCI. However, neither PKMzeta nor phosphorylation of PKMzeta was changed after tGCI or HPC. The results of the present study are consistent with the hypothesis that both enhanced recovery of Na(+)/K(+)-ATPase activity due to preserved the protein levels of Na(+)/K(+)-ATPase alpha1 subunit and reduced DNA fragmentation after tGCI contribute to the protection afforded by HPC. However, PKMzeta activation does not appear to play a role in this neuroprotection.
机译：我们先前证明，在短暂性全脑缺血（tGCI）10分钟之前1天应用30分钟的低氧预处理（HPC）可以减少成年大鼠海马CA1区域的神经元丢失。本研究的目的是研究Na（+）/ K（+）-ATPase和蛋白激酶Mzeta（PKMzeta）在HPC对成年大鼠的tGCI的保护作用中的作用。我们发现tGCI 10分钟后，海马CA1子区域Na（+）/ K（+）-ATPase的活性下降。在成年大鼠中，HPC 30分钟后未见此效果。对应于Na（+）/ K（+）-ATPase活性的变化，HPC后，Na（+）/ K（+）-ATPase alpha1亚基的表面表达增加。此外，HPC显着减少了tGCI后海马CA1子区域中末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）阳性细胞的数量。但是，tGCI或HPC后，PKMzeta和PKMzeta的磷酸化均未改变。本研究的结果与假说相符，即由于保留了Na（+）/ K（+）-ATPase alpha1亚基的蛋白质水平而降低了Na（+）/ K（+）-ATPase活性并增强了还原tGCI后的DNA片段有助于HPC提供保护。但是，PKMzeta激活似乎在这种神经保护中没有作用。

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