亚慢性睡眠碎片化诱导雄性大鼠内分泌改变及抑郁样行为

文献信息

中文摘要

背景： 睡眠碎片化是阻塞性睡眠呼吸暂停（OSA）的标志性特征，已通过神经内分泌调节紊乱与情绪障碍相关联。然而，反复睡眠碎片化后抑郁样行为和激素变化的时间依赖性发展仍不清楚。本研究考察了反复实验性睡眠碎片化对雄性Wistar大鼠抑郁样行为和内分泌状态的影响。
方法： 将24只雄性Wistar大鼠随机分配到三个实验组（每组n = 8）：跑台对照（TC；静止跑台）、活动对照（AC；10分钟奔跑/30分钟休息循环）和睡眠碎片化（SF；30秒奔跑/90秒休息循环）。在光照期前6小时内每天连续14天实施处理。在第1、7和14天通过强迫游泳试验评估抑郁样行为。全程监测体重，并在终点测量血清皮质酮和睾酮。睡眠结构由跑台方案推断，而非直接记录。
结果： SF大鼠在14天内表现出不动时间逐渐增加以及游泳和攀爬减少，反映抑郁样行为的逐渐出现。与对照组相比，SF动物还表现出体重增长显著降低、皮质酮升高（p < 0.01）和睾酮降低（p < 0.001）。
结论： 亚慢性睡眠碎片化诱导了进行性抑郁样表型，并伴有神经内分泌改变，提示与OSA相关的反复睡眠中断可能促成抑郁相关的内分泌失调。由于睡眠结构未被直接记录且激素仅在终点测量，这些发现应解释为关联性而非机制性。

英文摘要

BACKGROUND: Sleep fragmentation, a hallmark of obstructive sleep apnea (OSA), has been linked to mood disorders through disrupted neuroendocrine regulation. However, the time-dependent development of depression-like behaviors and hormonal changes following recurrent sleep fragmentation remains unclear. This study examined the effects of repeated experimental sleep fragmentation on depression-like behavior and endocrine status in male Wistar rats.
METHODS: Twenty-four male Wistar rats were randomly assigned to three experimental groups (n = 8 per group): treadmill control (TC; stationary treadmill), activity control (AC; 10-min running/30-min resting cycles), and sleep fragmentation (SF; 30-s running/90-s resting cycles). Treatments were applied daily for 14 consecutive days during the first 6 h of the light phase. Depression-like behavior was assessed via the forced swimming test on days 1, 7, and 14. Body weight was monitored throughout, and serum corticosterone and testosterone were measured at the endpoint. Sleep architecture was inferred from the treadmill protocol rather than directly recorded.
RESULTS: SF rats showed progressive increases in immobility and decreases in swimming and climbing over 14 days, reflecting the gradual emergence of depression-like behavior. SF animals also exhibited significantly reduced body-weight gain, elevated corticosterone (p < 0.01), and reduced testosterone (p < 0.001) compared with controls.
CONCLUSIONS: Subchronic sleep fragmentation induced a progressive depression-like phenotype accompanied by neuroendocrine alterations, suggesting that recurrent sleep interruptions relevant to OSA may contribute to depression-associated endocrine dysregulation. Because sleep architecture was not directly recorded and hormones were measured only at the endpoint, these findings should be interpreted as associative rather than mechanistic.