Hydrogen Gas Treatment Improves the Neurological Outcome After Traumatic Brain Injury Via Increasing miR-21 Expression.
Lu Wang, Chongfa Zhao, Shuang Wu, Guanghui Xiao, Xin Zhuge, Ping Lei, Keliang Xie · Shock (Augusta, Ga.) · 2018
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 a laboratory model, H₂ treatment decreased the levels of oxidative products (malondialdehyde and 8-iso-prostaglandin F2α) and increased the activities of endogenous antioxidant enzymes (superoxide dismutase and catalase) in brain after TBI, which were prevented by miR-21 antagomir. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.
What the Researchers Tested
The study examined in vitro cell-culture laboratory experiment.
How Molecular Hydrogen Was Used
H₂ treatment was given by exposure to 2% H₂ from 30 min to 5 h after TBI operation.
What Molecular Hydrogen Changed
Here, the researchers found that H₂ treatment significantly increased the expression of miR-21 in brain from 6 h to 3 d after TBI. The level of miR-21 expression in brain was significantly decreased after intracerebroventricular infusion of miR-21 antagomir in TBI-challenged rats with or without H₂ treatment. The researchers found that H₂ treatment conferred a better neurological outcome after TBI by improving neurological dysfunction, alleviating brain edema as well as decreasing lesion volume and blood-brain barrier permeability, which were significantly prevented by miR-21 antagomir.
H₂ Mechanisms / Biological Findings
The source material reviewed did not establish a specific molecular hydrogen mechanism for the reported findings.
Authors’ Conclusion
The authors concluded that taken together, these data indicate that H₂ treatment improves the neurological outcome after TBI via increasing miR-21 expression.