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
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 rat CPB model and an in vitro cell hypoxia model were established, 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. The authors concluded that the PI3K/Akt/GSK3β signaling pathway plays an important role in the mechanism of CPB-induced brain injury. These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
What the Findings Mean
H2HUBB reviewed how molecular hydrogen affected the outcomes measured in A rat CPB model and an in vitro cell hypoxia model were established. 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.
What the Researchers Studied
The researchers studied A rat CPB model and an in vitro cell hypoxia model were established. The study used a in vitro cell-culture laboratory experiment.
What Effects Did Molecular Hydrogen Have?
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. The authors concluded that the PI3K/Akt/GSK3β signaling pathway plays an important role in the mechanism of CPB-induced brain injury.
Why These Findings Matter
These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
How Strong Is This Evidence?
This is laboratory evidence from a in vitro cell-culture laboratory experiment. It is most informative for the biological mechanisms, cellular responses, or biochemical outcomes directly measured.
Technical Study Details
H2HUBB classifies this publication as laboratory study with laboratory or cellular evidence. The research population or model was A rat CPB model and an in vitro cell hypoxia model were established. The study used a in vitro cell-culture laboratory experiment.
Limitations and Safety
No separate limitations or safety findings were identified in the current-study 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.