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缺血预处理可减少沙土鼠海马CA1神经元中氧糖剥夺诱导的细胞内锌积累。

Ischemic preconditioning decreases intracellular zinc accumulation induced by oxygen-glucose deprivation in gerbil hippocampal CA1 neurons.

作者信息

Miyawaki Takahiro, Yokota Hidenori, Oguro Keiji, Kato Kengo, Shimazaki Kuniko

机构信息

Department of Surgical Neurology, Jichi Medical School, Minamikawachi-machi, Tochigi 329-0498, Japan.

出版信息

Neurosci Lett. 2004 May 27;362(3):216-9. doi: 10.1016/j.neulet.2004.03.030.

Abstract

In normal gerbils, intracellular zinc ions ([Zn2+]i) and calcium ions ([Ca2+]i) accumulate in hippocampal CA1 neurons after global ischemia. We examined whether ischemic preconditioning modifies these changes in gerbil hippocampal slices. In normal slices, large increases in [Zn2+]i and [Ca2+]i were observed in the stratum radiatum of the CA1 area after oxygen-glucose deprivation. In preconditioned slices, there were significantly decreased peak levels of [Zn2+]i and [Ca2+]i in CA1. However, there were no differences in the peak levels of these ions in CA3 and dentate gyrus. These results suggest that modified [Zn2+]i and [Ca2+]i accumulation after an ischemic insult might be important for the mechanisms of ischemic tolerance induced by preconditioning.

摘要

在正常沙鼠中,全脑缺血后海马CA1神经元内的锌离子([Zn2+]i)和钙离子([Ca2+]i)会蓄积。我们研究了缺血预处理是否会改变沙鼠海马切片中的这些变化。在正常切片中,氧糖剥夺后CA1区辐射层的[Zn2+]i和[Ca2+]i大幅增加。在预处理切片中,CA1区[Zn2+]i和[Ca2+]i的峰值水平显著降低。然而,CA3区和齿状回中这些离子的峰值水平没有差异。这些结果表明,缺血性损伤后[Zn2+]i和[Ca2+]i蓄积的改变可能对预处理诱导的缺血耐受机制很重要。

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