General Research
Model: rat
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
Simplified Version Available
Hydrogen Therapy: A Promising Solution for Reducing Brain Injury During Surgery
A study found that hydrogen-rich saline reduced brain injury in rats undergoing cardiopulmonary bypass. The solution worked by activating a special pathway in the body that prevents cell death and reduces inflammation. This discovery could lead to a simple and effective way to improve outcomes for patients undergoing heart surgery.
Read Simplified ArticleAbstract
Publish Year 2017 Country China Rank Positive Journal Cellular Physiology and Biochemistry Primary Topic Brain Secondary TopicSurgery/Transplantation Model Rat Tertiary TopicCardiopulmonary Bypass Vehicle Saline (Dissolved) pH Neutral Application Mixed Comparison Complement
Methods
Results: After CPB, brain tissue anatomy was disordered, and cell structure was abnormal. 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. After adding the PI3K signaling pathway inhibitor, LY294002, to rat cerebral microvascular endothelial cells (CMECs), HRS could reduce activated Akt expression and downstream regulatory gene phosphorylation of GSK3β expression, and inhibit CMEC apoptosis.
Results
Conclusion: 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.