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Oxidative Stress Parameters in Different Brain Structures Following Lateral Fluid Percussion Injury in the Rat

机译:大鼠侧脑液Per打损伤后不同脑结构的氧化应激参数

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摘要

Free radicals mediated damage of phospholipids, proteins and nucleic acids results in subsequent neuronal degeneration and cell loss. Aim of this study was to evaluate the existence of lipid and protein oxidative damage and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in various rat brain structures 24 h after lateral fluid percussion brain injury (LFPI). Parietal cortex, hippocampus, thalamus, entorhinal cortex, and cerebellum from the ipsilateral hemisphere were processed for analyses of the thiobarbituric acid reactive substances (TBARS) and oxidized protein levels as well as for the SOD and GSH-Px activities. Immunohistochemical detection of oxidized proteins was also performed. Results of our study showed that LFPI caused significant oxidative stress in the parietal cortex and hippocampus while other brain regions tested in this study were not oxidatively altered by LFPI. GSH-Px activities were significantly increased in the parietal cortex and hippocampus, while the SOD activities remained unchanged following LFPI in all regions investigated.
机译:自由基介导的磷脂,蛋白质和核酸的损伤导致随后的神经元变性和细胞损失。这项研究的目的是评估在侧脑液冲击性脑损伤(LFPI)后24小时内各种大鼠脑结构中脂质和蛋白质氧化损伤的存在以及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性。处理来自同侧半球的顶叶皮层,海马,丘脑,内嗅皮层和小脑,以分析硫代巴比妥酸反应性物质(TBARS)和氧化蛋白水平以及SOD和GSH-Px活性。还进行了氧化蛋白质的免疫组织化学检测。我们的研究结果表明,LFPI会在顶叶皮层和海马中引起明显的氧化应激,而本研究中测试的其他大脑区域不会被LFPI氧化改变。在所有研究区域中,LFPI后顶叶皮层和海马中的GSH-Px活性显着增加,而SOD活性保持不变。

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