Traumatic brain injury (TBI) is a public health problem in which even though 80 to 90% of cases are considered mild, usually starts a sequence of neurological disorders that can last a considerable time. Most of the research of this injury has been focused on oxidative stress and functional deficits; however, mechanisms that underlie the development of neuropsychiatric disorders remain little researched. Due to this, the present authors decided to investigate whether recurrent concussion protocols alter depressive-like phenotype behavior, and whether mitochondria play an indispensable role in this behavior or not. The experimental data revealed, for the first time, that the present protocol of recurrent concussions (4, 7, and 10 injuries) in mice did not alter immobility time during tail suspension tests (TSTs), but decreased hippocampal mitochondrial respiration and increased expression of proteins such as nuclear factor erythroid 2-related factor 2 (Nrf2) and superoxide (SOD2). This experimental data suggests that bioenergetic changes elicited by recurrent concussion did not induce depressive-like behavior, but activated the transcription factor of responsive antioxidant elements (ARE) that delay or prevent secondary cascades in this neurological disease.

中文翻译：

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线粒体生物能学和氧化应激在小鼠复发性脑震荡模型抑郁行为中的作用

创伤性脑损伤 (TBI) 是一个公共卫生问题，尽管 80% 至 90% 的病例被认为是轻微的，但通常会引发一系列可能持续相当长一段时间的神经系统疾病。大多数关于这种损伤的研究都集中在氧化应激和功能缺陷上。然而，神经精神疾病发展的机制仍然很少被研究。因此，本作者决定研究反复脑震荡方案是否会改变抑郁样表型行为，以及线粒体是否在这种行为中发挥不可或缺的作用。实验数据首次显示，目前对小鼠进行反复脑震荡（4、7 和 10 次损伤）的方案并没有改变尾悬试验 (TST) 期间的不动时间，但减少了海马线粒体呼吸并增加了核因子红细胞 2 相关因子 2 (Nrf2) 和超氧化物 (SOD2) 等蛋白质。该实验数据表明，反复脑震荡引起的生物能量变化不会诱发抑郁样行为，而是激活反应性抗氧化元件（ARE）的转录因子，从而延迟或防止这种神经系统疾病的继发级联反应。