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Effect of the mitochondrial antioxidant, Mito Vitamin E, on hypoxic-ischemic striatal injury in neonatal rats: a dose-response and stereological study.

机译:线粒体抗氧化剂线粒体维生素E对新生大鼠缺氧缺血性纹状体损伤的作用:剂量反应和体视学研究。

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摘要

A mitochondria-targeted antioxidant, Mito Vitamin E (MitoVit E), has previously been shown to prevent mitochondrial oxidative damage. The aim of this study was to investigate the effect of MitoVit E on neuronal survival in the rat striatum after acute perinatal hypoxia-ischemia. Continuous striatal infusion with 4.35 microM, 43.5 microM, or 148 microM of MitoVit E before, during, and after hypoxia-ischemia was not neuroprotective for striatal medium-spiny neurons. Pre- or posttreatment with 435 microM MitoVit E was neurotoxic. These results suggest that MitoVit E is not significantly neuroprotective for striatal medium-spiny neurons after acute perinatal hypoxic-ischemic brain injury. The results also suggest that mitochondrial oxidative damage does not contribute significantly to the death of striatal medium-spiny neurons after perinatal hypoxia-ischemia.
机译:线粒体靶向抗氧化剂,Mito维生素E(MitoVit E),先前已证明可预防线粒体的氧化损伤。这项研究的目的是研究MitoVit E对急性围产期缺氧缺血后大鼠纹状体神经元存活的影响。在缺氧缺血之前,期间和之后,连续用4.35 microM,43.5 microM或148 microM的MitoVit E进行纹状体输注对纹状体中棘神经元没有神经保护作用。 435 microM MitoVit E的预处理或后处理具有神经毒性。这些结果表明,MitoVit E对急性围产期缺氧缺血性脑损伤后的纹状体中棘神经元没有明显的神经保护作用。结果还表明,围产期缺氧缺血后,线粒体的氧化损伤对纹状体中多刺神经元的死亡没有明显贡献。

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