Selenium has been shown to possess antioxidant and neuroprotective effects by modulating mitochondrial function and activating mitochondrial biogenesis. Our previous study has also suggested that selenium protected neurons against glutamate toxicity and hyperglycemia-induced damage by regulating mitochondrial fission and fusion. However, it is still not known whether the mitochondrial biogenesis is involved in selenium alleviating hyperglycemia-aggravated cerebral ischemia reperfusion (I/R) injury. The object of this study is to define whether selenium protects neurons against hyperglycemia-aggravated cerebral I/R injury by promoting mitochondrial biogenesis. In vitro oxygen deprivation plus high glucose model decreased cell viability, enhanced reactive oxygen species production, and meanwhile stimulated mitochondrial biogenesis signaling. Pretreated with selenium significantly decreased cell death and further activated the mitochondrial biogenesis signaling. In vivo 30 min of middle cerebral artery occlusion in the rats under hyperglycemic condition enhanced neurological deficits, enlarged infarct volume, exacerbated neuronal damage and oxidative stress compared with normoglycemic ischemic rats after 24 h reperfusion. Consistent to the in vitro results, selenium treatment alleviated ischemic damage in hyperglycemic ischemic animals. Furthermore, selenium reduced the structural changes of mitochondria caused by hyperglycemic ischemia and further promoted the mitochondrial biogenesis signaling. Selenium activates mitochondrial biogenesis signaling, protects mitochondrial structure integrity and ameliorates cerebral I/R injury in hyperglycemic rats.

中文翻译：

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硒中线粒体生物合成的参与可减少高血糖症加重的脑缺血损伤。

硒已经显示出通过调节线粒体功能和激活线粒体生物发生而具有抗氧化和神经保护作用。我们以前的研究还表明，硒可通过调节线粒体的裂变和融合来保护神经元免受谷氨酸毒性和高血糖引起的损伤。然而，线粒体的生物发生是否与硒减轻高血糖症加重的脑缺血再灌注（I / R）损伤有关尚不清楚。这项研究的目的是确定硒是否通过促进线粒体生物发生来保护神经元免受高血糖加重的脑I / R损伤。体外缺氧加高糖模型降低了细胞活力，增加了活性氧的产生，同时刺激了线粒体的生物发生信号。硒预处理可显着降低细胞死亡，并进一步激活线粒体生物发生信号。与正常血糖缺血大鼠相比，高血糖条件下大鼠体内大脑中动脉闭塞30分钟可增加神经功能缺损，梗塞体积增大，神经元损伤加重和氧化应激，而再灌注24 h后较之。与体外结果一致，硒治疗减轻了高血糖缺血动物的缺血损伤。此外，硒减少了由高血糖缺血引起的线粒体的结构变化，并进一步促进了线粒体的生物发生信号。硒可激活线粒体生物发生信号，保护线粒体结构完整性，并改善高血糖大鼠的脑I / R损伤。