Hydrogen gas alleviates sepsis-induced neuroinflammation and cognitive impairment through regulation of DNMT1 and DNMT3a-mediated BDNF promoter IV methylation in mice.
Mingdong Yu, Chao Qin, Pei Li, Yingli Zhang, Ying Wang, Jing Zhang, Dedong Li, Huixing Wang, Yuechun Lu, Keliang Xie, Yang Yu, Yonghao Yu · International immunopharmacology · 2021
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Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
The researchers found that 2% H₂ inhalation can reduce pro-inflammatory factors, alleviate DNMT1, DNMT3a but not DNMT3b expression, make hypomethylation of BDNF promoter IV at 5 CpG sites, enhance the BDNF levels and then decrease escape latency but increase platform crossing times in septic mice. These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential within the outcomes and biological pathways measured in this model.
What the Findings Mean
H2HUBB reviewed how molecular hydrogen was evaluated in this publication and summarizes the source-grounded findings below. The researchers found that 2% H₂ inhalation can reduce pro-inflammatory factors, alleviate DNMT1, DNMT3a but not DNMT3b expression, make hypomethylation of BDNF promoter IV at 5 CpG sites, enhance the BDNF levels and then decrease escape latency but increase platform crossing times in septic mice.
What the Researchers Studied
The study used a preclinical animal experiment.
What Effects Did Molecular Hydrogen Have?
Source-reported hydrogen concentration: 2% source-reported H₂ gas concentration; Source-reported hydrogen exposure: 2% source-reported H₂ gas concentration. The researchers found that 2% H₂ inhalation can reduce pro-inflammatory factors, alleviate DNMT1, DNMT3a but not DNMT3b expression, make hypomethylation of BDNF promoter IV at 5 CpG sites, enhance the BDNF levels and then decrease escape latency but increase platform crossing times in septic mice. The authors concluded that 2% H₂ inhalation may alleviate SAE through altering the regulation of BDNF promoter IV methylation which mediated by DNMT1 and DNMT3a in the hippocampus of septic mice. Sepsis-associated encephalopathy (SAE) can cause acute and long-term cognitive impairment and increase the mortality rate in sepsis patients, and the researchers previously reported that 2% hydrogen gas (H₂) inhalation has a therapeutic effect on SAE, but the underlying mechanism remains unclear.
Why These Findings Matter
These preclinical findings add evidence supporting molecular hydrogen's therapeutic potential within the outcomes and biological pathways measured in this model.
How Strong Is This Evidence?
This is preclinical animal evidence from a preclinical animal experiment. It is most informative for the disease model, mechanisms, biomarkers, and outcomes directly measured in the study.
Technical Study Details
H2HUBB classifies this publication as animal study with preclinical animal evidence. The study used a preclinical animal experiment. The source-reported hydrogen concentration was 2% source-reported H₂ gas concentration.
Limitations and Safety
No separate limitations or safety findings were identified in the source text available to H2HUBB.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.