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首页> 外文期刊>Neural regeneration research >Potential targets for protecting against hippocampal cell apoptosis after transient cerebral ischemia-reperfusion injury in aged rats
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Potential targets for protecting against hippocampal cell apoptosis after transient cerebral ischemia-reperfusion injury in aged rats

机译:预防老年大鼠短暂性脑缺血再灌注损伤后海马细胞凋亡的潜在靶点

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Mitochondria play an important role in neuronal apoptosis caused by cerebral ischemia, and the role is mediated by the expression of mitochondrial proteins. This study investigated the involvement of mitochondrial proteins in hippocampal cell apoptosis after transient cerebral ischemia-reperfusion injury in aged rats using a comparative proteomics strategy. Our experimental results show that the aged rat brain is sensitive to ischemia-reperfusion injury and that transient ischemia led to cell apoptosis in the hippocampus and changes in memory and cognition of aged rats. Differential proteomics analysis suggested that this phenomenon may be mediated by mitochondrial proteins associated with energy metabolism and apoptosis in aged rats. This study provides potential drug targets for the treatment of transient cerebral ischemia-reperfusion injury.
机译:线粒体在由脑缺血引起的神经元凋亡中起重要作用,并且该作用由线粒体蛋白的表达介导。本研究采用比较蛋白质组学方法研究了老年大鼠短暂性脑缺血再灌注损伤后线粒体蛋白参与海马细胞凋亡的情况。我们的实验结果表明,老年大鼠大脑对缺血-再灌注损伤敏感,短暂性缺血导致海马细胞凋亡以及老年大鼠记忆力和认知能力的改变。差异蛋白质组学分析表明,这种现象可能是由与衰老大鼠能量代谢和凋亡相关的线粒体蛋白介导的。该研究为治疗短暂性脑缺血-再灌注损伤提供了潜在的药物靶标。

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