Hydrogen Gas Protects Hearts from Chronic Failure in Rats
- Authors
- Jing Chi, Zizhuo Li, Xiaojian Hong, Tong Zhao, Yueyue Bie, Wen Zhang, Jiaxing Yang, Ziming Feng, Zhouqi Yu, Qiannan Xu, Luqi Zhao, Weifan Liu, Yunan Gao, Hongxiao Yang, Jiemei Yang, Jiaren Liu, Wei Yang
- Journal
- Frontiers in Physiology
- Year
- 2018
- DOI
- 10.3389/fphys.2018.01026
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Chronic Heart Failure
- Body System
- Cardiovascular
TL;DR
Breathing in molecular hydrogen (H2) gas helps delay the worsening of chronic heart failure in rats by protecting the heart from oxidative stress and cell death.
Key Finding
Inhaling hydrogen gas improved heart function and reduced oxidative stress and cell death in rats with chronic heart failure, with the protective effect linked to suppression of the p53 protein.
Summary
This study tested whether inhaling hydrogen gas could help rats with chronic heart failure (a condition where the heart weakens and can't pump blood effectively). Researchers found that rats breathing hydrogen gas showed improved heart function and had less cellular damage from oxidative stress (harmful molecules that damage cells) and apoptosis (programmed cell death). The protective effect appeared to work by reducing activity of a protein called p53 that triggers cell death.
Practical Takeaway
While this rat study suggests hydrogen inhalation may have protective effects against heart failure progression, it is not yet evidence that this would work in humans. The study was conducted only in animals, so results cannot be directly applied to human health. More research, including human trials, would be needed before hydrogen therapy could be considered a viable treatment for heart failure.
Abstract
Background: Continuous damage from oxidative stress and apoptosis are the important mechanisms that facilitate chronic heart failure (CHF). Molecular hydrogen (H2) has potentiality in the aspects of anti-oxidation. The objectives of this study were to investigate the possible mechanism of H2 inhalation in delaying the progress of CHF. Methods and Results: A total of 60 Sprague-Dawley (SD) rats were randomly divided into four groups: Sham, Sham treated with H2, CHF and CHF treated with H2. Rats from CHF and CHF treated with H2 groups were injected isoprenaline subcutaneously to establish the rat CHF model. One month later, the rat with CHF was identified by the echocardiography. After inhalation of H2, cardiac function was improved vs. CHF (p < 0.05), whereas oxidative stress damage and apoptosis were significantly attenuated (p < 0.05). In this study, the mild oxidative stress was induced in primary cardiomyocytes of rats, and H2 treatments significantly reduced oxidative stress damage and apoptosis in cardiomyocytes (p < 0.05 or p < 0.01). Finally, as a pivotal transcription factor in reactive oxygen species (ROS)-apoptosis signaling pathway, the expression and phosphorylation of p53 were significantly reduced by H2 treatment in this rat model and H9c2 cells (p < 0.05 or p < 0.01). Conclusion: As a safe antioxidant, molecular hydrogen mitigates the progression of CHF via inhibiting apoptosis modulated by p53. Therefore, from the translational point of view and speculation, H2 is equipped with potential therapeutic application as a novel antioxidant in protecting CHF in the future.