Hydrogen inhalation protects hypoxic-ischemic brain damage by attenuating inflammation and apoptosis in neonatal rats.
Guojiao Wu, Zhiheng Chen, Peipei Wang, Mingyi Zhao, Masayuki Fujino, Chen Zhang, Wenjuan Zhou, Shin-Ichi Hirano, Xiao-Kang Li, Lingling Zhao · Experimental biology and medicine (Maywood, N.J.) · 2019
Research-use notice
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
In rats, hypoxia–ischemia induced neuronal damage and increased the expression of the apoptotic factors, P-JNK, and p53, which were attenuated by hydrogen inhalation (P < 0.05). 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 hydrogen-rich water affected the outcomes measured in rats. Hypoxia–ischemia induced neuronal damage and increased the expression of the apoptotic factors, P-JNK, and p53, which were attenuated by hydrogen inhalation (P < 0.05).
What the Researchers Studied
The researchers studied rats. The study used a preclinical animal experiment.
What Effects Did Molecular Hydrogen Have?
Source-reported hydrogen concentration: 3% source-reported H₂ gas concentration; Source-reported hydrogen exposure: 3% source-reported H₂ gas concentration; reported treatment duration: 90 min. Hypoxia–ischemia induced neuronal damage and increased the expression of the apoptotic factors, P-JNK, and p53, which were attenuated by hydrogen inhalation (P < 0.05). The authors concluded that in conclusion, hypoxia–ischemia induced severe long-term damage to the brain, which could be alleviated by hydrogen inhalation in a time-dependent manner. Hypoxia–ischemia injury induced the inflammatory response of microglia; however, these changes were inhibited by hydrogen inhalation. Hydrogen (H₂) is an antioxidant that can be used to treat HIBD; however, the mechanism by which hydrogen may be used as a promising treatment for neonates with HIBD is not very clear.
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 research population or model was rats. The study used a preclinical animal experiment. The hydrogen delivery method was hydrogen-rich water. The source-reported hydrogen concentration was 3% source-reported H₂ gas concentration. The reported treatment duration was 90 min.
Limitations and Safety
Safety information: Moreover, neither is easy to control the thera- peutic concentration, nor can instrument accurately mea- sure the concentration of H 2S in cells, it is difficult to track and analyze the effects of H 2S.33 Compared to H2S, H₂ is a safe and stable molecular free radicals’ scav- enger odor, which can be measured easily and accurately.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base. The original scholarly source is available at https://www.ebm-journal.org/journals/experimental-biology-and-medicine/articles/10.1177/1535370219855399/pdf.