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Sleep deprivation (SD) has become a universal social problem. There is a causal relationship between SD and energy metabolism disorder. Phytochemicals have been demonstrated to have excellent sleep-promoting effects, and studies have shown that ginsenoside Rg5 (Rg5) exerts sedative and hypnotic effects. The present study aimed to investigate the role of Rg5 in regulating energy metabolism and explore the potential mechanism of improving sleep. Sleep-deprived rats were randomly divided into a control group (Ctrl), SD model group (SD), Rg5 group (GRg5), and melatonin group (MT). Sleep-deprived model rats were generated by housing rats in an SD box for 4 weeks. The Ctrl and SD groups were given equal volumes of saline. The Rg5 groups were given 25mg/kg Rg5 or 50mg/kg Rg5, and the MT group was given 0.27g/kg MT. A Western blot analysis and ELISA were used to detect the metabolic levels, mitochondrial functional proteins, AMPK pathway proteins, clock-related proteins, adenosine receptors, and neurotransmitter receptors. The results showed that Rg5 corrected abnormal glucose and lipid metabolism as well as improved ATP levels. In addition, Rg5 alleviated mitochondrial structural damage and improved the expression of proteins involved in mitochondrial biosynthesis, fission, and fusion. Moreover, Rg5 improved the expression of AMPK/PGC-1/Nrf-1 pathway proteins, regulated mitochondrial biological functions, and affected the rhythm characteristics of circadian clock-related proteins. Further, Rg5 improved the expression of A₁R and A${}_{2\mathrm{\text{A}}}$R as well as regulated the expression levels of GABAA1$\alpha$ and mGluR5 to improve sleep in SD rats.

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Sleep deprivation has been reported to be a contributing factor for the epidemic of obesity. However, it is still largely unknown how sleep deprivation contributes to obesity at the transcriptional level. Here, we identified the significantly changed genes and pathways that may contribute to the sleep deprivation-induced obesity by analyzing two online datasets, including mouse obesity database and mouse sleep deprivation database. 298 differentially expressed genes (DEGs) were identified in high fat diet mice as compared to normal diet mice, while 541 DEGs were identified in mice with sleep deprivation when compared with mice with normal sleep. There are 12 common DEGs, such as Saa3 and Plin4, in both comparisons. And six of common DEGs were validated in other Gene Expression Omnibus (GEO) dataset. GO and KEGG pathway analyses revealed 19 common altered pathways, and most of them were metabolic processes, including steroid metabolic process, small molecule metabolic process and cholesterol metabolic process. Notably, we found that Aldoc, Cyp2b10, Nsdhl, Pcsk9, Saa3, Plin4 and Acss2 were involved in most of those altered pathways. Taken together, our study suggests that Saa3, Plin4, Aldoc, Cyp2b10, Nsdhl, Pcsk9 and Acss2 might be involved in sleep deprivation-induced obesity by regulating metabolic processes.

The hippocampus is the brain structure that is responsible for the formation of learning memories. Sleep disorders leading to cognitive impairment are strongly associated with the hippocampus. Phototherapy offers a new physical therapy for the treatment of sleep disorders, with the advantages of being noninvasive and having few side effects. However, the mechanism by which phototherapy improves cognitive impairment caused by sleep disorders remains unclear. In this study, we used phototherapy combined with optogenetic technology to investigate the effect of noninvasive phototherapy on cognitive functions in sleep-deprived mice. Our results suggest that phototherapy might improve cognitive functions in sleep-deprived mice by modulating the hippocampus. Our study expands the research progress on noninvasive phototherapy for the treatment of sleep disorders.