Hydrogen Gas Protects Brain Cells from Oxygen Damage During Surgery
- Authors
- Rong Wei, Rufang Zhang, Yewei Xie, Li Shen, Fang Chen
- Journal
- Cellular Physiology and Biochemistry
- Year
- 2015
- DOI
- 10.1159/000430122
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Hypoxia/Reoxygenation Injury
- Body System
- Nervous System
TL;DR
Hydrogen gas can protect brain cells from damage caused by oxygen deprivation and subsequent reoxygenation by reducing harmful oxidative stress and altering certain microRNA levels.
Key Finding
Hydrogen treatment significantly reduced brain cell death caused by oxygen deprivation and restoration by lowering harmful oxidative stress and suppressing specific microRNA molecules that trigger cell death.
Summary
This laboratory study examined whether hydrogen gas dissolved in liquid could protect brain cells from damage caused by oxygen deprivation followed by oxygen restoration—a condition that occurs during certain heart surgeries. Researchers exposed cultured brain cells to this oxygen-deprivation cycle and found that hydrogen treatment reduced cell death by decreasing harmful molecules called reactive oxygen species (unstable atoms that damage cells) and by affecting specific genetic regulators called microRNAs.
Practical Takeaway
While these results are promising, this study was conducted in laboratory-grown cells only, not in living organisms or humans. The findings suggest hydrogen may have potential protective effects for brain tissue during certain surgical procedures, but much more research—including animal studies and human trials—would be needed before any clinical applications could be considered.
Abstract
Background & Aims: Deep hypothermic circulatory arrest (DHCA) is a cerebral protection technique that has been used in the operations involving the aortic arch and brain aneurysm for decades. We previous showed that DHCA treated rats developed a significant oxidative stress and apoptosis in neurons. We here intend to investigate the protective the effect of hydrogen against oxidative stress-induced cell injury and the involved mechanisms using an in vitro experimental model of hypoxia/reoxygenation (H/R) on HT-22 cells. Methods: The model of H/R was established using an airtight culture container and the anaeropack. Measurement of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) production was used H2DCFDA and JC-1 staining. Western blot was used for the quantification of Akt, p-Akt, Bcl-2, Bax and cleaved caspase-3 proteins. The microRNA (miRNA) profile in hippocampal neurons from rat model of DHCA was determined by miRNA deep sequencing. Results: The elevation of ROS and reduction of MMP were significantly induced by the treatment with hypoxia for 18 h followed by reoxygenation for 6 h. Hydrogen treatment significantly reduced H/R-caused cell death. The levels of p-Akt (Ser 473) and Bcl-2 were significantly increased while Bax and cleaved caspase-3 were decreased by hydrogen treatment on the model of H/R. The expression of miR-200 family was significantly elevated in model of DHCA and H/R. Hydrogen administration inhibited the H/R-induced expression of miR-200 family in HT-22 cells. In addition, inhibition of miR-200 family suppressed H/R-caused cell death through reducing ROS production. Conclusions: These results suggest that H/R causes oxidative stress-induced cell death and that the hydrogen protects against H/R-induced cell death in HT22 cells, in part, due to reducing expression of miR-200 family.