Hydrogen Therapy Protects Heart from Sleep Apnea Damage in Rats
- Authors
- Ji-Xian Song, Hong-Yu Han, Qing-Qing Liu, Meng-Fan Sun, Bo-Han Yu, Ya-Shuo Zhao, Ya-Jing Guo, En-Sheng Ji
- Journal
- International Immunopharmacology
- Year
- 2025
- DOI
- 10.1016/j.intimp.2025.115974
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Obstructive Sleep Apnea
- Body System
- Cardiovascular
TL;DR
Hydrogen protected the heart from sleep apnea–related damage by reducing oxidative stress and preventing ferroptosis through activation of cellular defense pathways.
Key Finding
Hydrogen gas reduced heart cell damage from chronic intermittent hypoxia by activating the Nrf2 protein pathway, which decreased oxidative stress and promoted cellular cleanup processes.
Summary
This study tested whether hydrogen could protect heart cells from damage caused by chronic intermittent hypoxia (repeated periods of low oxygen, similar to what happens in sleep apnea). Researchers used rat models and heart cells in the lab, and found that hydrogen reduced a type of cell damage called ferroptosis by activating a protein called Nrf2, which helps cells manage stress and clean up damaged parts. The protective effects disappeared when researchers blocked this pathway, suggesting hydrogen works specifically through this mechanism.
Practical Takeaway
This is early laboratory and animal research suggesting hydrogen may have potential for protecting heart tissue during conditions like sleep apnea that involve repeated oxygen drops. However, these findings are from rat studies and cell cultures, not human trials, so it's unclear whether hydrogen would have the same effects in people or what dose would be needed. More research, including human studies, would be necessary before drawing conclusions about hydrogen's usefulness for sleep apnea or heart health.
Abstract
Objective: Obstructive sleep apnea (OSA) is a common disorder for which comprehensive and effective treatments and interventions have not yet been fully developed. A hallmark of OSA is chronic intermittent hypoxia (CIH), which significantly contributes to the pathogenesis of cardiovascular diseases through mechanisms such as ferroptosis. Hydrogen is known for its selective antioxidant properties, however its inhibitory effects on CIH-induced ferroptosis and the associated molecular mechanisms remain insufficiently characterized. This study aims to elucidate the effects of hydrogen on CIH-induced ferroptosis and to explore the potential molecular pathways involved. Methods: In vivo and in vitro CIH models were established to observe changes in cardiac function and pathological damage. Use transcriptomics analysis to identify potential targets. Additionally, probes, electron microscopy, and related assay kits were employed to assess oxidative stress and ferroptosis. Results: Hydrogen could mitigate cardiac injury and ferroptosis induced by CIH, primarily through its sustained modulation of oxidative stress and the activation of autophagy. Hydrogen has been observed to reduce ferroptosis in H9C2 cells induced by RSL3, with effects comparable to those of Mito Q, Fer-1, and the Nrf2 activator SA. Importantly, the protective effects of hydrogen against ferroptosis were negated by the application of the autophagy inhibitor 3-MA, the Nrf2 inhibitor ML385 and si-Nfe2l2 gene. Conclusion: These findings suggested that hydrogen could promote autophagy and reduce oxidative stress by activating the Nrf2 protein, thereby inhibiting ferroptosis and alleviating cardiac damage caused by CIH.