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Tat-DJ-1 通过增加抗氧化水平来保护兔脊髓腹角神经元免受缺血性损伤。

Tat-DJ-1 protects neurons from ischemic damage in the ventral horn of rabbit spinal cord via increasing antioxidant levels.

机构信息

Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul, 151-742, South Korea.

出版信息

Neurochem Res. 2014 Jan;39(1):187-93. doi: 10.1007/s11064-013-1205-y. Epub 2013 Nov 29.

DOI:10.1007/s11064-013-1205-y
PMID:24293249
Abstract

The DJ-1 gene is highly conserved in diverse species and DJ-1 is known as an anti-oxidative stress factor. In this study, we investigated the neuroprotective effects of DJ-1 against ischemic damage in the rabbit spinal cord. Tat-DJ-1 fusion proteins were constructed to facilitate the penetration of DJ-1 protein into the neurons. Tat-1-DJ-1 fusion protein was administered to the rabbit 30 min after ischemia/reperfusion, and transient spinal cord ischemia was induced by occlusion of the aorta at the subrenal region for 15 min. The administration of Tat-DJ-1 significantly improved the Tarlov score compared to that in the Tat (vehicle)-treated group at 24, 48 and 72 h after ischemia/reperfusion. At 72 h after ischemia/reperfusion, the number of cresyl violet-positive neurons was significantly increased in the Tat-DJ-1-treated group compared to that in the vehicle-treated group. Lipid peroxidation as judged from the malondialdehyde levels was significantly decreased in the Tat-DJ-1-treated group compared to that in the vehicle-treated group. In contrast, superoxide dismutase and catalase levels were significantly increased in the Tat-DJ-1-treated group compared to that in the vehicle-treated group. This result suggests that DJ-1 protects neurons from ischemic damage in the ventral horn of the spinal cord via its antioxidant effects.

摘要

DJ-1 基因在多种物种中高度保守,DJ-1 被认为是一种抗氧化应激因子。在这项研究中,我们研究了 DJ-1 对兔脊髓缺血损伤的神经保护作用。构建了 Tat-DJ-1 融合蛋白,以促进 DJ-1 蛋白进入神经元。在缺血/再灌注 30 分钟后,向兔给予 Tat-DJ-1 融合蛋白,并通过在肾下区域阻断主动脉 15 分钟来诱导短暂性脊髓缺血。与 Tat(载体)处理组相比,Tat-DJ-1 给药在缺血/再灌注后 24、48 和 72 小时显著改善了 Tarlov 评分。在缺血/再灌注后 72 小时,与载体处理组相比,Tat-DJ-1 处理组的甲苯胺蓝阳性神经元数量显著增加。丙二醛水平判断的脂质过氧化明显低于载体处理组。相比之下,Tat-DJ-1 处理组的超氧化物歧化酶和过氧化氢酶水平明显高于载体处理组。这一结果表明,DJ-1 通过其抗氧化作用保护脊髓腹角的神经元免受缺血损伤。

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Neuroprotective effects of PEP-1-Cu,Zn-SOD against ischemic neuronal damage in the rabbit spinal cord.
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