Hydrogen Therapy Slows Blood Vessel Aging from Sleep Apnea
- Authors
- Dongli Li, Qingqing Liu, Xintong Fan, Kerong Qi, Mengfan Sun, Jixian Song, Yajing Guo, Ensheng Ji
- Journal
- European Journal of Pharmacology
- Year
- 2025
- DOI
- 10.1016/j.ejphar.2025.178078
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Obstructive Sleep Apnea
- Body System
- Cardiovascular
TL;DR
Hydrogen therapy may protect blood vessels from aging damage caused by sleep apnea by reducing oxidative stress and boosting cellular cleanup processes.
Key Finding
Molecular hydrogen gas reduced signs of blood vessel aging and improved vascular function in mice exposed to chronic intermittent hypoxia, working through a cellular pathway that reduces oxidative stress and activates cellular cleanup mechanisms.
Summary
This study used mice to investigate whether molecular hydrogen (a gas with antioxidant properties) could help protect blood vessels from damage caused by chronic intermittent hypoxia—a condition that mimics obstructive sleep apnea, where oxygen levels drop repeatedly during sleep. Researchers found that hydrogen gas improved blood vessel function, reduced cellular aging markers, and activated a cellular cleanup process called autophagy, suggesting it may help prevent vascular aging associated with sleep apnea.
Practical Takeaway
While this mouse study suggests hydrogen gas may help protect blood vessels from sleep apnea-related damage, it is early-stage research that has not been tested in humans. The findings are preliminary and would need human clinical trials to determine whether hydrogen water or gas could actually benefit people with sleep apnea or vascular aging.
Abstract
Obstructive sleep apnea (OSA), characterized by recurrent upper airway collapse during sleep, has been linked to systemic physiological impairment and accelerated vascular senescence through chronic intermittent hypoxia (CIH). Currently, there is no approved medication to treat the complications of OSA. Molecular hydrogen (H2), an anti-oxidative therapeutic agent, plays an important role in regulating cardiovascular and anti-aging. In this study, we aimed to investigate the therapeutic effect of H2 on OSA-associated vascular endothelial aging by establishing a mouse model induced by CIH and explore the mechanism of H2 from the perspective of oxidative stress and autophagy. Echocardiography and aortic ring vasodilatory response were employed to assess the impact of H2 on the aortic function in CIH mice. Haematoxylin and eosin staining, transmission electron microscopy, SA-β-gal staining, DHE staining, and immunofluorescence staining were utilized to observe the changes in histopathology and protein expression. The results demonstrated that H2 alleviated CIH-induced vascular endothelial aging by improving the pathological injury of the aorta, alleviating vasodilation dysfunction, decreasing the expression of oxidative stress and aging markers, and increasing the expression of autophagy-related proteins. Mechanism investigations revealed that H2 could inhibit oxidative stress and activate autophagy pathways, but silencing Nuclear factor-erythroid 2 related factor 2 (Nrf2) impaired the ability of H2 to ameliorate endothelial senescence in the CIH cell model. These suggest that H2 can activate mitochondrial autophagy, reduce oxidative stress, and improve the senescence of endothelial cells induced by CIH, providing evidence for the clinical application of H2 in OSA-related vascular endothelial senescence diseases.