睡眠剥夺对亚健康形成的影响及相关机制

[目的]探索睡眠剥夺(SD)对亚健康形成的影响和作用,研究睡眠剥夺对脑功能的影响及机制。[方法]在开展亚健康主症特征的1000例人群调查基础上,建立大鼠SD实验模型,通过观察大鼠的行为学变化考察睡眠剥夺对大鼠应激能力的影响,测试大鼠的Y-迷宫实验成绩考察睡眠剥夺对大鼠脑认知功能的影响,观察大鼠海马结构一氧化氮合酶(NOS)活性与神经元型一氧化氮合酶(nNOS)蛋白表达水平的变化,研究睡眠剥夺对脑体功能影响的作用机制。[结果]学生人群以睡眠障碍为第一症状表现,其后才是疲劳主症;农民则以疲劳为第一症状表现,睡眠障碍排在第2位,提示睡眠障碍在亚健康表现中占据有重要地位。大鼠在实验性睡眠剥夺后行为表现出抑制性,应激能力下降;睡眠剥夺可使大鼠Y-迷宫测试成绩下降(P<0.05),海马结构的NOS活性和nNOS蛋白表达减少(P<0.05),损害学习记忆等脑认知能力。[结论]睡眠障碍是亚健康表现的首要症状,睡眠剥夺可使机体脑功能处于低下状态,表明睡眠剥夺对亚健康形成和发展有重要影响和作用,其机制可能与下调海马结构NOS、nNOS表达水平有关。

Effects of Sleep Deprivation (SD) on Sub-clinical Condition and Its Correlative Mechanisms

[Objective] To explore the influence of sleep deprivation (SD) on sub-clinical condition and cerebral function and interpret the possible mechanism.[Methods] Based on the investigation of main symptom of sub-clinical condition in about one thousand persons, the SD model in rats was made and their behavior was researched to explore the effect of SD on the stress ability. Y-lost palace test was adopted to research the influence of SD on the ability of cognition of brain. The activity of NOS and the levels of protein expression of nNOS in hippocampus of rats were researched to explore the action and the mechanism of SD on the function of brain and body.[Results] In the group of students, the first symptom was sleep-disorder and then fatigue; In the group of farmers, however, the first symptom was fatigue and the second sleep-disorder, indicating the sleep-disorder played an important role in sub-clinical state. In the research of rats, it was found that after sleep deprivation, the behavior of rats became inhibited, the stress ability became lowered. SD could reduce the results of Y-lost palace test (P<0.05), reduce the levels of NOS and nNOS in hippocampus of rats (P<0.05) and result in the injury of the function of cognition of brain, such as learning and memory.[Conclusions] Sleep-disorder is the main symptom of the sub-clinical state. SD can make the function of brain lowed. It is indicated that SD plays an important role in the formation and development of sub-clinical state. Its mechanism may be related to the reducing of the levels of NOS and the protein expression of nNOS in hippocampus.