Transcriptome analysis of cardiac tissues from mice subjected to SD model with oxygen therapy

Adequate sleep is essential for relieving stress and rejuvenating the mind; however, undesirable physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly common. However, the influence of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially on cardiac diseases remain controversial. Here, we constructed the experimental SD model in mice and found it significantly resulted in weakness, depression-like behaviors, and multiple organs dysfunction. Intriguingly, SD mice developed pathogenic cardiac hypertrophy and fibrosis with poor ejection fraction as well as fractional shortening. 16s rRNA sequencing demonstrated that SD-induced the pathogenic effects of gut microbiota, which was also observed in mice received by fecal microbe from SD mice in fecal microbiota transplantation (FMT) assays. Next, we investigated the therapeutic effects and underlying mechanisms of oxygen therapy in gut microbiota-associated cardiac fibrosis and dysfunction. The environment of 30% oxygen concentration effectively ameliorated the pathological effects on cardiac function. Transcriptome data also found oxygen therapy targeted several hypoxia-dependent pathways and suppressed cardiac collagen production. In conclusion, these results indicated the importance of sufficient sleep in gut microbiota and may represent a potential therapeutic strategy of oxygen environment exerts protective effects in sleepless sufferings through gut microbiota. Sleep deprivation was conducted using a water tank-based sleep deprivation (SD) equipment, involving 18 hours of deprivation per day for 4 weeks. The starting light time (ZT0) was consistently set at 07:00, regardless of the photoperiod length, and the sleep deprivation period was scheduled from ZT7 (14:00) to the following ZT1 (08:00). During the experiment, after the mice completed sleep deprivation at ZT1, thet were placed in an oxygen chamber. 30% oxygen concentrations were adjusted using the contronlling panel, and the mice were treated for 2 hrs. At the end of the treatment, the mice were returned to their cages for rest and subsequently subjected to sleep deprivation at ZT7 for 18 hours. The blank control group did not receive any additional interventions and was maintained under normal conditions.