Hydrogen Gas Protects Brain After Stroke by Reducing Cell Death
- Authors
- Zheng Peng, Xiao-Jian Li, Yan Zhou, Jia-Tong Zhang, Qi Zhu, Jia-Qing Sun, Chun-Hua Hang, Wei Li, Qing-Rong Zhang, Zong Zhuang
- Journal
- Free Radical Biology and Medicine
- Year
- 2024
- DOI
- 10.1016/j.freeradbiomed.2024.02.028
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Subarachnoid Hemorrhage
- Body System
- Nervous System
TL;DR
Breathing hydrogen gas can help protect the brain and improve recovery after a type of stroke known as subarachnoid hemorrhage by reducing brain cell death and inflammation.
Key Finding
Hydrogen gas improved motor function, sensory function, and cognitive ability in mice after subarachnoid hemorrhage, while reducing harmful nerve cell damage and brain inflammation.
Summary
This study examined whether hydrogen gas could protect the brain after a type of stroke called subarachnoid hemorrhage (bleeding in the space around the brain). Researchers exposed mice to hydrogen gas and found that it improved their movement, sensation, and memory after the stroke. Hydrogen appeared to work by reducing harmful iron-related damage to nerve cells and decreasing brain inflammation.
Practical Takeaway
This early research in mice suggests hydrogen may have protective effects for brain injury from hemorrhagic stroke, but these are animal-only findings with unknown study duration and sample size. Human clinical trials would be needed before any conclusions about hydrogen's usefulness for stroke patients could be drawn.
Abstract
Objective: Spontaneous subarachnoid hemorrhage (SAH), the third most common stroke subtype, is associated with high mortality and disability rates. Therefore, finding effective therapies to improve neurological function after SAH is critical. The objective of this study was to investigate the potential neuroprotective effects of hydrogen in the context of SAH, specifically, by examining its role in attenuating neuronal ferroptosis and inhibiting neuroinflammation, which are exacerbated by excess iron ions after SAH. Methods: Mice were exposed to chambers containing 3% hydrogen, and cells were cultured in incubators containing 60% hydrogen. Neurological function in mice was assessed using behavioral scores. Protein changes were detected using western blotting. Inflammatory factors were detected using enzyme linked immunosorbent assay. Probes, electron microscopy, and related kits were employed to detect oxidative stress and ferroptosis. Results: Hydrogen improved the motor function, sensory function, and cognitive ability of mice after SAH. Additionally, hydrogen facilitated Nuclear factor erythroid 2 -related factor 2 activation, upregulated Glutathione peroxidase 4, and inhibited Toll-like receptor 4, resulting in downregulation of inflammatory responses, attenuation of oxidative stress after SAH, and inhibition of neuronal ferroptosis. Conclusion: Hydrogen exerts neuroprotective effects by inhibiting neuronal ferroptosis and attenuating neuroinflammation after SAH. Keywords: Ferroptosis; Hydrogen; Neuroinflammation; Nrf2; Subarachnoid hemorrhage.