Hydrogen Gas Protects Heart During Heart Attack Treatment in Rats
- Authors
- Chaoqun Nie, Xue Ding, Rong A, Min Zheng, Zhenning Li, Shuang Pan, Wei Yang
- Journal
- Life Sciences
- Year
- 2021
- DOI
- 10.1016/j.lfs.2021.119248
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Myocardial Ischemia-Reperfusion Injury
- Body System
- Cardiovascular
TL;DR
Breathing in hydrogen gas can significantly reduce heart damage and improve heart function after a heart attack by decreasing oxidative stress and inflammation.
Key Finding
Hydrogen gas inhalation significantly reduced heart damage and improved cardiac function in rats experiencing ischemia-reperfusion injury (the damage that occurs when blood flow is restored after a heart attack) by decreasing oxidative stress and blocking a cell-death pathway called NLRP3-mediated pyroptosis.
Summary
This study tested whether breathing hydrogen gas could protect rat hearts from damage that occurs when blood flow is restored after a heart attack. Researchers found that rats that inhaled hydrogen gas had smaller areas of heart damage, better heart function, and reduced markers of cellular stress compared to rats that did not receive hydrogen. The protective effects appeared to work by reducing harmful molecules called free radicals and preventing a type of cell death called pyroptosis.
Practical Takeaway
While this rat study suggests hydrogen gas may help protect heart tissue during reperfusion therapy, it is early-stage research that has not been tested in humans. The findings are interesting for understanding potential mechanisms, but much more research—including human clinical trials—would be needed before hydrogen therapy could be considered a viable treatment for heart disease. This study alone cannot support health claims about hydrogen water or gas for cardiac protection in people.
Abstract
Aims: Reperfusion therapy is the most common and effective treatment against ischemic heart disease (IHD), but the process inflicts massive ischemia/reperfusion (I/R) injury for which no treatment exists. Notably, reperfusion after ischemia causes ischemia/reperfusion injury (IR injury) and the 'no-reflow' phenomenon seriously affecting the therapeutic effects in clinical practice. The principle purpose of this study is to validate the effect of hydrogen gas on IHD and further explore the mechanism of hydrogen gas in alleviating myocardial I/R injury and no-reflow phenomenon. Materials and methods: The rat model of myocardial ischemia-reperfusion was well established. Myocardial infarct size was evaluated by TTC & Evans blue staining. The no-reflow area and the cardiac function were assessed by thioflavin-S staining and echocardiography respectively. Microstructure and mitochondria of myocardial tissue were assessed by transmission electron microscope. Western blot and immunohistochemistry were used to evaluate the expression of NLRP3 mediated pyroptosis related proteins. The 8-OHdG, MDA and serum total ROS were used to evaluate the degree of oxidative stress. Key findings: The myocardial infarct size, no-reflow area, cardiac function, microstructure and mitochondrial morphology of I/R model rats were significantly improved after hydrogen inhalation. In addition, the expression of 8-OHdG, MDA, ROS and NLRP3 mediated pyroptosis related proteins were significantly decreased. Significance: We found that oxidative stress and NLRP3 mediated pyroptosis are the important mechanisms for hydrogen to alleviate myocardial I/R injury, and we also confirmed that hydrogen can significantly improve no reflow phenomenon caused by ischemia-reperfusion.