Hydrogen Gas Protects Brain Cells from Stroke Damage in Lab Study
- Authors
- Ya-Hong Li, Shun Zhang, Lu Tang, Jianguo Feng, Jing Jia, Ye Chen, Li Liu, Jun Zhou
- Journal
- Journal of Personalized Medicine
- Year
- 2023
- DOI
- 10.3390/jpm13040631
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cerebral Ischemia/Reperfusion Injury
- Body System
- Nervous System
TL;DR
Hydrogen gas (H2) can protect brain cells from damage caused by stroke-like conditions, potentially through a specific pathway involving a long non-coding RNA and a protein that regulates cell survival and inflammation.
Key Finding
Hydrogen gas protected brain cells from oxygen-glucose deprivation injury by activating a specific cellular pathway (lincRNA-EPS/Sirt1/autophagy) that reduced inflammation and cell death.
Summary
This laboratory study examined how hydrogen gas protects brain cells from injury caused by oxygen and blood flow loss (a condition that mimics stroke). Researchers treated cultured brain cells with hydrogen and found it reduced cell death, decreased inflammation, and prevented programmed cell death. The protection appeared to work through activation of specific cellular pathways involving a regulatory molecule called lincRNA-EPS.
Practical Takeaway
While this early laboratory study suggests hydrogen may have neuroprotective mechanisms against stroke-like injury, it was conducted only in cultured cells, not in living organisms or humans. Much more research, including animal studies and human trials, would be needed before any health claims could be made about hydrogen's effectiveness for stroke prevention or treatment.
Abstract
Cerebral ischemia/reperfusion (CI/R) injury causes high disability and mortality. Hydrogen (H2) enhances tolerance to an announced ischemic event; however, the therapeutic targets for the effective treatment of CI/R injury remain uncertain. Long non-coding RNA lincRNA-erythroid prosurvival (EPS) (lincRNA-EPS) regulate various biological processes, but their involvement in the effects of H2 and their associated underlying mechanisms still needs clarification. Herein, we examine the function of the lincRNA-EPS/Sirt1/autophagy pathway in the neuroprotection of H2 against CI/R injury. HT22 cells and an oxygen-glucose deprivation/reoxygenation (OGD/R) model were used to mimic CI/R injury in vitro. H2, 3-MA (an autophagy inhibitor), and RAPA (an autophagy agonist) were then administered, respectively. Autophagy, neuro-proinflammation, and apoptosis were evaluated by Western blot, enzyme-linked immunosorbent assay, immunofluorescence staining, real-time PCR, and flow cytometry. The results demonstrated that H2 attenuated HT22 cell injury, which would be confirmed by the improved cell survival rate and decreased levels of lactate dehydrogenase. Furthermore, H2 remarkably improved cell injury after OGD/R insult via decreasing pro-inflammatory factors, as well as suppressing apoptosis. Intriguingly, the protection of H2 against neuronal OGD/R injury was abolished by rapamycin. Importantly, the ability of H2 to promote lincRNA-EPS and Sirt1 expression and inhibit autophagy were abrogated by the siRNA-lincRNA-EPS. Taken together, the findings proved that neuronal cell injury caused by OGD/R is efficiently prevented by H2 via modulating lincRNA-EPS/Sirt1/autophagy-dependent pathway. It was hinted that lincRNA-EPS might be a potential target for the H2 treatment of CI/R injury.