Hydrogen Gas Protects Heart from Damage After Heart Attack in Rats
- Authors
- Shuang Pan, Bin Wang, Mengshu Yu, Jiawen Zhang, Bowei Fan, Chaoqun Nie, Rentong Zou, Xinrui Yang, Zhuoqun Zhang, Xiaojian Hong, Wei Yang
- Journal
- Free Radical Research
- Year
- 2025
- DOI
- 10.1080/10715762.2025.2474014
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Myocardial Infarction
- Body System
- Cardiovascular
TL;DR
Breathing in hydrogen gas can reduce heart damage and improve heart function in rats after a heart attack by decreasing harmful oxidative stress and improving cell survival.
Key Finding
Hydrogen inhalation reduced heart tissue damage after myocardial infarction in rats by restoring mitochondrial function and reducing harmful free radicals (ROS).
Summary
Researchers studied whether hydrogen gas could help protect heart tissue after a heart attack in rats. They found that rats that received hydrogen inhalation had smaller areas of damaged heart tissue, better-functioning mitochondria (the energy-producing parts of cells), and lower levels of harmful molecules called free radicals compared to rats that had a heart attack without hydrogen treatment.
Practical Takeaway
This rat study suggests hydrogen gas may help protect heart tissue after a heart attack by working at the cellular level, but human studies are needed before any conclusions can be drawn about its use in people. The study is preliminary and focused on understanding the biological mechanism rather than testing safety or effectiveness in patients.
Abstract
Background: Acute myocardial infarction (AMI) is a deadly cardiovascular disease with no effective solution except for percutaneous coronary intervention and coronary artery bypass grafting. Inflammation and apoptosis of the injured myocardium after revascularization seriously affect the prognosis. Hydrogen possesses anti-inflammatory, anti-oxidative, and anti-apoptotic effects and may become a new treatment for AMI. This study explored the specific mechanism by which hydrogen operates during AMI treatment. Methods: Thirty Sprague-Dawley rats were randomly divided into three groups: control, myocardial infarction (MI), and myocardial infarction + hydrogen (MI+H2), each containing 10 rats. The MI rat model was established by ligation of the left anterior descending branch. The MI+H2 group received 2% hydrogen inhalation treatment for 3 h/Bid. Results: Myocardial infarct size was evaluated using triphenyl tetrazolium chloride staining. Transmission electron microscopy showed reduced mitochondrial damage compared with the MI group. JC-1 staining, which indicates mitochondrial membrane potential, showed a low red/green fluorescence intensity ratio in the MI group compared to that in the control group, indicating mitochondrial membrane potential loss. After hydrogen inhalation, this ratio increased, suggesting partial recovery of membrane potential. In addition, mitochondrial ATP content, mitochondrial complex I, and mitochondrial complex III activity were significantly decreased in the MI group, which was improved after hydrogen administration. Western blotting analysis showed decreased Cyt-c protein levels in the myocardial mitochondria and increased levels in the cytoplasm of MI rats. Following hydrogen inhalation, the levels of ROS, 8-OHdG, and MDA that could represent oxidative stress injury significantly decreased. Besides, the expression of Cyt-C, Bax, cleaved-caspase-9, and cleaved-caspase-3 in MI group significantly increased, while the Bcl-2, TRX2, SOD2 expression decreased. The expression of these proteins in MI+H2 group was improved compared with the MI group. Conclusion: Overall, hydrogen inhalation reduces myocardial infarct size, improves mitochondrial dysfunction, and modulates the levels of apoptosis-related substances. Importantly, Hydrogen reduces acute myocardial infarction damage by downregulating ROS and upregulating antioxidant proteins.