PDF(Pubmed)
Abstract：
Sleep deprivation is highly prevalent in the modern world, possibly reaching epidemic proportions. While multiple theories regarding the roles of sleep exist (inactivity, energy conservation, restoration, brain plasticity and antioxidant), multiple unknowns still remain regarding the proposed antioxidant roles of sleep. The existing experimental evidence is often contradicting, with studies pointing both toward and against the presence of oxidative stress after sleep deprivation. The main goals of this review were to analyze the existing experimental data regarding the relationship between sleep deprivation and oxidative stress, to attempt to further clarify multiple aspects surrounding this relationship and to identify current knowledge gaps. Systematic searches were conducted in three major online databases for experimental studies performed on rat models with oxidative stress measurements, published between 2015 and 2022. A total of 54 studies were included in the review. Most results seem to point to changes in oxidative stress parameters after sleep deprivation, further suggesting an antioxidant role of sleep. Alterations in these parameters were observed in both paradoxical and total sleep deprivation protocols and in multiple rat strains. Furthermore, the effects of sleep deprivation seem to extend beyond the central nervous system, affecting multiple other body sites in the periphery. Sleep recovery seems to be characterized by an increased variability, with the presence of both normalizations in some parameters and long-lasting changes after sleep deprivation. Surprisingly, most studies revealed the presence of a stress response following sleep deprivation. However, the origin and the impact of the stress response during sleep deprivation remain somewhat unclear. While a definitive exclusion of the influence of the sleep deprivation protocol on the stress response is not possible, the available data seem to suggest that the observed stress response may be determined by sleep deprivation itself as opposed to the experimental conditions. Due to this fact, the observed oxidative changes could be attributed directly to sleep deprivation.
摘要：
睡眠不足在现代世界非常普遍，可能达到流行病的程度。虽然存在关于睡眠作用的多种理论(不活动，节能，restoration,大脑可塑性和抗氧化剂)，关于睡眠的抗氧化作用，仍然有许多未知因素。现有的实验证据往往是矛盾的，研究表明睡眠剥夺后存在氧化应激。这篇综述的主要目的是分析现有的关于睡眠剥夺和氧化应激之间关系的实验数据，试图进一步澄清围绕这种关系的多个方面，并确定当前的知识差距。在三个主要的在线数据库中进行了系统搜索，以对具有氧化应激测量的大鼠模型进行实验研究。在2015年至2022年之间发布。共纳入54项研究。大多数结果似乎指向睡眠剥夺后氧化应激参数的变化，进一步暗示了睡眠的抗氧化作用。在矛盾和完全睡眠剥夺方案以及多种大鼠品系中都观察到了这些参数的变化。此外，睡眠剥夺的影响似乎超出了中枢神经系统，影响外围多个其他身体部位。睡眠恢复的特征似乎是变异性增加，同时存在一些参数的正常化和睡眠剥夺后的长期变化。令人惊讶的是,大多数研究表明，睡眠不足后存在应激反应。然而,睡眠剥夺期间应激反应的起源和影响尚不清楚.虽然最终排除睡眠剥夺方案对应激反应的影响是不可能的，现有数据似乎表明，观察到的应激反应可能是由睡眠剥夺本身决定的，而不是实验条件。由于这一事实,观察到的氧化变化可直接归因于睡眠剥夺。
