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兔短暂性脊髓缺血后运动神经元中帕金森病相关蛋白的诱导

Induction of Parkinson disease-related proteins in motor neurons after transient spinal cord ischemia in rabbits.

作者信息

Sakurai Masahiro, Kawamura Takae, Nishimura Hidekazu, Suzuki Hiroyoshi, Tezuka Fumiaki, Abe Koji

机构信息

Department of Cardiovascular Surgery, National Hospital Organization Sendai Medical Center, Miyagino, Sendai, Japan.

出版信息

J Cereb Blood Flow Metab. 2009 Apr;29(4):752-8. doi: 10.1038/jcbfm.2008.167. Epub 2009 Jan 14.

Abstract

The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. We investigated a possible mechanism of neuronal death by immunohistochemical analysis for DJ-1, PINK1, and alpha-Synuclein. We used a 15-min rabbit spinal cord ischemia model, with use of a balloon catheter. Western blot analysis for DJ-1, PINK1, and alpha-Synuclein; temporal profiles of DJ-1, PINK1, and alpha-Synuclein immunoreactivity; and double-label fluorescence immunocytochemical studies were performed. Western blot analysis revealed scarce immunoreactivity for DJ-1, PINK1, and alpha-Synuclein in the sham-operated spinal cords. However, they became apparent at 8 h after transient ischemia, which returned to the baseline level at 1 day. Double-label fluorescence immunocytochemical study revealed that both DJ-1 and PINK1, and DJ-1 and alpha-Synuclein were positive at 8 h of reperfusion in the same motor neurons, which eventually die. The induction of DJ-1 and PINK1 proteins in the motor neurons at the early stage of reperfusion may indicate oxidative stress, and the induction of alpha-Synuclein may be implicated in the programmed cell death change after transient spinal cord ischemia.

摘要

脊髓损伤的机制一直被认为与脊髓运动神经元细胞对缺血的易损性有关。然而,这种易损性的机制尚未完全明确。我们通过对DJ-1、PINK1和α-突触核蛋白进行免疫组织化学分析,研究了神经元死亡的一种可能机制。我们使用球囊导管建立了一个15分钟的兔脊髓缺血模型。进行了针对DJ-1、PINK1和α-突触核蛋白的蛋白质免疫印迹分析;检测了DJ-1、PINK1和α-突触核蛋白免疫反应性的时间变化情况;并开展了双标记荧光免疫细胞化学研究。蛋白质免疫印迹分析显示,在假手术的脊髓中,DJ-1、PINK1和α-突触核蛋白的免疫反应性很弱。然而,在短暂缺血后8小时它们变得明显,并在1天时恢复到基线水平。双标记荧光免疫细胞化学研究显示,在最终死亡的同一运动神经元中,DJ-1和PINK1以及DJ-1和α-突触核蛋白在再灌注8小时时均呈阳性。再灌注早期运动神经元中DJ-1和PINK1蛋白的诱导可能表明存在氧化应激,而α-突触核蛋白的诱导可能与短暂性脊髓缺血后的程序性细胞死亡变化有关。

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