Hydrogen Research Study
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Preclinical animal evidenceAnimal studyOther or not reported

Hydrogen alleviated cognitive impairment and blood‒brain barrier damage in sepsis-associated encephalopathy by regulating ABC efflux transporters in a PPARα-dependent manner.

Yuanyuan Bai, Wen Mi, Xiaoyin Meng, Beibei Dong, Yi Jiang, Yuechun Lu, Yonghao Yu · BMC neuroscience · 2023

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Independent study record

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H2HUBB Research Library branded molecular hydrogen research image
Primary topic Cognitive Health and Neurodegeneration
Evidence type Preclinical animal evidence
Publication type Animal study
Hydrogen method Other or not reported

H2HUBB TAKEAWAY

Hydrogen improved survival, reduced brain dysfunction, and decreased inflammatory cytokines in the experimental sepsis model. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.

What the Researchers Studied

The study examined mice.

How Molecular Hydrogen Was Used

After injection with DMSO/GW6471 (a PPARα inhibitor), the mice subjected to sham/caecal ligation and puncture (CLP) surgery were treated with H₂ for 60 min postoperation.

What the Researchers Found

Finally, the researchers found that H₂ improved survival rates and brain dysfunction and decreased inflammatory cytokines. H₂ decreased water content in the brain and EB extravasation and increased ZO-1, occludin, VE-cadherin and ABC efflux transporters regulated by PPARα. Thus, the researchers concluded that H₂ decreases BBB permeability to protect against brain dysfunction in sepsis; this effect is mediated by PPARα and its regulation of ABC efflux transporters.

H₂ Mechanisms / Biological Findings

Hydrogen (H₂) can protect against blood‒brain barrier (BBB) damage in sepsis-associated encephalopathy (SAE), but the mechanism is still unclear.

Authors’ Conclusion

The authors concluded that the researchers concluded that H₂ decreases BBB permeability to protect against brain dysfunction in sepsis; this effect is mediated by PPARα and its regulation of ABC efflux transporters.