Hydrogen Saline Protects Brain During Heart Surgery in Rats
- Authors
- Keyan Chen, Nan Wang, Yugang Diao, Wanwei Dong, YingJie Sun, Lidan Liu, Xiuying Wu
- Journal
- Cellular Physiology and Biochemistry
- Year
- 2017
- DOI
- 10.1159/000484024
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Brain Injury
- Body System
- Neurological
TL;DR
A hydrogen-rich solution can reduce brain damage caused by heart surgery involving cardiopulmonary bypass by affecting a specific cell signaling pathway.
Key Finding
Hydrogen-rich saline reduced brain injury markers and cell death in rats undergoing cardiopulmonary bypass surgery, with effects mediated through the PI3K/Akt/GSK3β signaling pathway.
Summary
This rat study tested whether hydrogen-rich saline (a salt solution containing dissolved hydrogen gas) could protect the brain from injury during heart-lung bypass surgery. Researchers found that the hydrogen-rich saline reduced brain swelling, decreased cell death, and lowered inflammation markers in treated rats compared to untreated controls. The protective effect appeared to work through a specific cellular pathway (PI3K/Akt/GSK3β) that regulates cell survival.
Practical Takeaway
While this rat study suggests hydrogen-rich saline may protect brain tissue during cardiac surgery, it is early-stage research that has not been tested in humans. The findings are interesting for potential future clinical applications, but much more research would be needed before any health recommendations could be made for surgical patients.
Abstract
Background/aims: Cardiopulmonary bypass (CPB) is prone to inducing brain injury during open heart surgery. A hydrogen-rich solution (HRS) can prevent oxidation and apoptosis, and inhibit inflammation. This study investigated effects of HRS on brain injury induced by CPB and regulatory mechanisms of the PI3K/Akt/GSK3β signaling pathway. Methods: A rat CPB model and an in vitro cell hypoxia model were established. After HRS treatment, Rat behavior was measured using neurological deficit score; Evans blue (EB) was used to assess permeability of the blood-brain barrier (BBB); HE staining was used to observe pathological changes; Inflammatory factors and brain injury markers were detected by ELISA; the PI3K/Akt/GSK3β pathway-related proteins and apoptosis were assessed by western blot, immunohistochemistry and qRT -PCR analyses of brain tissue and neurons. 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. 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.