Hydrogen Therapy Prevents Heart Damage from Sleep Disorder Breathing
- Authors
- Jixian Song, Qi Chen, Shan Xu, Yujing Guo, Yajing Guo, Cuiling Jia, Chenbing Zhao, Zhi Zhang, Boliang Li, Yashuo Zhao, Ensheng Ji
- Journal
- Current Issues in Molecular Biology
- Year
- 2023
- DOI
- 10.3390/cimb45120636
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cardiac Hypertrophy
- Body System
- Cardiovascular
TL;DR
Breathing hydrogen gas helps reduce heart enlargement and damage caused by intermittent low oxygen levels by improving iron balance and reducing oxidative stress in mice.
Key Finding
Hydrogen gas inhalation reduced heart enlargement caused by chronic low-oxygen exposure in mice by decreasing iron accumulation and oxidative stress in heart tissue.
Summary
This mouse study examined whether hydrogen gas could prevent heart enlargement caused by repeated episodes of low oxygen (a condition similar to sleep apnea). Researchers exposed mice to low-oxygen cycles and gave some of them hydrogen gas to breathe. They found that hydrogen reduced heart enlargement, decreased harmful molecules called free radicals, and lowered iron buildup in heart cells—all of which may have protected the heart from damage.
Practical Takeaway
While these results are promising, this is an animal study in mice, not humans. The findings suggest hydrogen may help protect hearts during repeated oxygen deprivation, but much more research—including human trials—would be needed before any health recommendations could be made. The specific mechanisms involved (iron metabolism and free radical reduction) may or may not translate to human physiology.
Abstract
The present study aimed to investigate the impact of hydrogen (H2) on chronic intermittent hypoxia (CIH)-induced cardiac hypertrophy in mice by modulating iron metabolism. C57BL/6N mice were randomly allocated into four groups: control (Con), CIH, CIH + H2, and H2. The mice were exposed to CIH (21-5% FiO2, 3 min/cycle, 8 h/d), and received inhalation of a hydrogen-oxygen mixture (2 h/d) for 5 weeks. Cardiac and mitochondrial function, levels of reactive oxygen species (ROS), and iron levels were evaluated. The H9C2 cell line was subjected to intermittent hypoxia (IH) and treated with H2. Firstly, we found H2 had a notable impact on cardiac hypertrophy, ameliorated pathological alterations and mitochondrial morphology induced by CIH (p < 0.05). Secondly, H2 exhibited a suppressive effect on oxidative injury by decreasing levels of inducible nitric oxide synthase (i-NOS) (p < 0.05) and 4-hydroxynonenal (4-HNE) (p < 0.01). Thirdly, H2 demonstrated a significant reduction in iron levels within myocardial cells through the upregulation of ferroportin 1 (FPN1) proteins (p < 0.01) and the downregulation of transferrin receptor 1 (TfR1), divalent metal transporter 1 with iron-responsive element (DMT1(+ire)), and ferritin light chain (FTL) mRNA or proteins (p < 0.05). Simultaneously, H2 exhibited the ability to decrease the levels of Fe2+ and ROS in H9C2 cells exposed to IH (p < 0.05). Moreover, H2 mediated the expression of hepcidin, hypoxia-inducible factor-1α (HIF-1α) (p < 0.01), and iron regulatory proteins (IRPs), which might be involved in the regulation of iron-related transporter proteins. These results suggested that H2 may be beneficial in preventing cardiac hypertrophy, a condition associated with reduced iron toxicity.