Chronic Sleep Deprivation Causes Anxiety, Depression and Impaired Gut Barrier in Female Mice-Correlation Analysis from Fecal Microbiome and Metabolome

慢性睡眠剥夺导致雌性小鼠焦虑、抑郁及肠道屏障受损——粪便微生物组和代谢组的相关性分析

阅读:6
作者:Lingyue Li, Zilin Meng, Yuebing Huang, Luyao Xu, Qianling Chen, Dongfang Qiao, Xia Yue

Background

Chronic sleep deprivation (CSD) plays an important role in mood disorders. However, the changes in the gut microbiota and metabolites associated with CSD-induced anxiety/depression-like behavior in female mice have not been determined. Due to the influence of endogenous hormone levels, females are more susceptible than males to negative emotions caused by sleep deprivation. Here, we

Conclusion

In summary, we found that CSD induced anxiety/depression-like behavior, caused gut microbiota dysbiosis, altered fecal metabolism, and damaged the colon barrier in female mice.

Methods

We used a 48-day sleep deprivation (SD) model using the modified multiple platform method (MMPM) to induce anxiety/depression-like behavior in female C57BL/6J mice and verified our

Results

Our study demonstrates that CSD induced anxiety/depressive-like behaviors in female mice. The results of 16S rDNA sequencing suggested that the relative abundance of the harmful bacteria g_ Rothia, g_ Streptococcus, g_ Pantoea, and g_ Klebsiella were significantly increased, while the beneficial bacteria g_ Rikenella, g_ Eubacterium]-xylanophilum-group, and g_ Eisenbergiella were significantly decreased after SD. Glycerophospholipid metabolism and glutathione metabolism were identified as key pathways in the fecal metabolism related to oxidative stress and inflammatory states of the intestine. Histological observation showed hyperplasia of epithelial cells, a decrease in goblet cells, and glandular atrophy of the colon in SD mice. There were correlations between some of the differential bacterial taxa, fecal metabolites, and behaviors.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。