Hydrogen-Rich Saline Attenuates Brain Injury Induced by Cardiopulmonary Bypass and Inhibits Microvascular Endothelial Cell Apoptosis Via the PI3K/Akt/GSK3β Signaling Pathway in Rats.
Keyan Chen, Nan Wang, Yugang Diao, Wanwei Dong, YingJie Sun, Lidan Liu, Xiuying Wu · Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
Hydrogen improved microvascular endothelial-cell viability partly through PI3K/Akt/GSK3β activation and inhibition of autophagy in a traumatic-brain-injury model. 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
A rat CPB model and an in vitro cell hypoxia model were established.
How Molecular Hydrogen Was Used
The source material available to H2HUBB did not provide enough detail to identify the molecular hydrogen administration method.
Laboratory Model
A rat CPB model and an in vitro cell hypoxia model were established.
What Molecular Hydrogen Changed
Brain tissue EB content increased. There was an increase in the number of apoptotic cells, an increase in expression of Bax and caspase-3, a decrease in expression of Bcl2, and increases in levels of Akt, GSK3β, P-Akt, and P-GSK3β in brain tissue. HRS treatment attenuated the inflammatory reaction,brain tissue EB content was significantly reduced and significantly decreased expression levels of Bax, caspase-3, Akt, GSK3β, P-Akt, and P-GSK3β in the brain.
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 the PI3K/Akt/GSK3β signaling pathway plays an important role in the mechanism of CPB-induced brain injury. HRS can reduce CPB-induced brain injury and inhibit CMEC apoptosis through the PI3K/Akt/GSK3β signaling pathway.