Cai Shuqi, Li Zixuan, Bai Jie, Ding Yue, Liu Ruisang, Fang Liben, Hou Dengyong, Zhang Sheng, Wang Xiaohui, Wang Yujia, Jiang Yuyu, Xiang Yan, Wu Wenhui, He Ying, Zhang Yunkai, Ren Xiaomeng
College of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Naval Medical Center, Naval Medical University, Shanghai, China.
Front Cell Infect Microbiol. 2025 Mar 5;15:1522431. doi: 10.3389/fcimb.2025.1522431. eCollection 2025.
Adequate sleep is of paramount importance for relieving stress and restoring mental vigor. However, the adverse physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly prevalent. Currently, the impact of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially cardiac diseases, remains controversial. Here, we employed the following methods: constructed an experimental sleep-deprivation model in mice; conducted 16S rRNA sequencing to investigate the changes in gut microbiota; through fecal microbiota transplantation (FMT) experiments, transplanted fecal microbiota from sleep-deprived mice to other mice; established an environment with a 30% oxygen concentration to explore the therapeutic effects of oxygen therapy on gut microbiota-associated cardiac fibrosis and dysfunction; and utilized transcriptome data to study the underlying mechanisms of oxygen therapy. The results revealed that: sleep-deprived mice exhibited weakness, depression-like behaviors, and dysfunction in multiple organs. Pathogenic cardiac hypertrophy and fibrosis occurred in sleep-deprived mice, accompanied by poor ejection fraction and fractional shortening. 16S rRNA sequencing indicated that sleep deprivation induced pathogenic effects on gut microbiota, and similar phenomena were also observed in mice that received fecal microbiota from sleep-deprived mice in the FMT experiments. The environment with a 30% oxygen concentration effectively alleviated the pathological impacts on cardiac function. Transcriptome data showed that oxygen therapy targeted several hypoxia-dependent pathways and inhibited the production of cardiac collagen. In conclusion, these results demonstrate the significance of sufficient sleep for gut microbiota and may represent a potential therapeutic strategy, where the oxygen environment exerts a protective effect on insomniacs through gut microbiota.
充足的睡眠对于缓解压力和恢复精神活力至关重要。然而，睡眠不足或睡眠剥夺（SD）所导致的不良生理和病理反应正变得越来越普遍。目前，睡眠不足对肠道微生物群以及与微生物群相关的人类疾病，尤其是心脏病的影响仍存在争议。在此，我们采用了以下方法：在小鼠中构建实验性睡眠剥夺模型；进行16S rRNA测序以研究肠道微生物群的变化；通过粪便微生物群移植（FMT）实验，将睡眠剥夺小鼠的粪便微生物群移植到其他小鼠体内；建立一个氧气浓度为30%的环境，以探索氧疗对肠道微生物群相关的心脏纤维化和功能障碍的治疗效果；并利用转录组数据研究氧疗的潜在机制。结果显示：睡眠剥夺的小鼠表现出虚弱、抑郁样行为以及多器官功能障碍。睡眠剥夺的小鼠出现病理性心脏肥大和纤维化，同时伴有射血分数和缩短分数降低。16S rRNA测序表明，睡眠剥夺对肠道微生物群产生了致病作用，在FMT实验中接受来自睡眠剥夺小鼠粪便微生物群的小鼠也观察到了类似现象。氧气浓度为30%的环境有效减轻了对心脏功能的病理影响。转录组数据表明，氧疗靶向了几个缺氧依赖途径并抑制了心脏胶原蛋白的产生。总之，这些结果证明了充足睡眠对肠道微生物群的重要性，并且可能代表一种潜在的治疗策略，即氧环境通过肠道微生物群对失眠者发挥保护作用。
