Effect of molecular hydrogen treatment on Sepsis‐Associated encephalopathy in mice based on gut microbiota

Introduction In our experiments, male wild‐type mice were randomly divided into four groups: the sham, SAE, SAE + 2% hydrogen gas inhalation (H2), and SAE + hydrogen‐rich water (HW) groups. The feces of the mice were collected for 16 S rDNA analysis 24 h after the models were established, and the se...

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Veröffentlicht in:CNS neuroscience & therapeutics 2023-02, Vol.29 (2), p.633-645
Hauptverfasser: Han, Qingqing, Bai, Yuanyuan, Zhou, Chunjing, Dong, Beibei, Li, Yingning, Luo, Ning, Chen, Hongguang, Yu, Yonghao
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Sprache:eng
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Zusammenfassung:Introduction In our experiments, male wild‐type mice were randomly divided into four groups: the sham, SAE, SAE + 2% hydrogen gas inhalation (H2), and SAE + hydrogen‐rich water (HW) groups. The feces of the mice were collected for 16 S rDNA analysis 24 h after the models were established, and the serum and brain tissue of the mice were collected for nontargeted metabolomics analysis. Aim Destruction of the intestinal microbiota is a risk factor for sepsis and subsequent organ dysfunction, and up to 70% of severely ill patients with sepsis exhibit varying degrees of sepsis‐associated encephalopathy (SAE). The pathogenesis of SAE remains unclear. We aimed to explore the changes in gut microbiota in SAE and the regulatory mechanism of molecular hydrogen. Results Molecular hydrogen treatment significantly improved the functional outcome of SAE and downregulated inflammatory reactions in both the brain and the gut. In addition, molecular hydrogen treatment improved gut microbiota dysbiosis and partially amended metabolic disorder after SAE. Conclusions Molecular hydrogen treatment promotes functional outcomes after SAE in mice, which may be attributable to increasing beneficial bacteria, repressing harmful bacteria, and metabolic disorder, and reducing inflammation. Molecular hydrogen treatment can significantly improve the gut microbiota and metabolites and reduce the inflammatory reaction and cognitive dysfunction after SAE. This study provides a basis for the pathogenesis and treatment of SAE.
ISSN:1755-5930
1755-5949
DOI:10.1111/cns.14043