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
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Independent study record
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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 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
Rats
How Molecular Hydrogen Was Used
This study demonstrated that inhaled H₂ is neuroprotective against HIBD in SpragueDawley rats by inhibiting the brain’s inflammatory response and neuronal apoptosis or damage and protecting against spatial memory decline. Further, this study showed that inhaled H₂ has potential as a therapeutic approach for HIBD.
What the Researchers Found
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).
Biological or Mechanistic Findings
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.
Authors’ Conclusion
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. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.