Hydrogen Therapy Protects Heart from Damage During Heart Attacks
- Authors
- Yue Zuo, Jiawei Wang, Zhexuan Gong, Yulong Wang, Qiang Wang, Xueyang Yang, Fulin Liu, Tongtong Liu
- Journal
- Journal of Cellular and Molecular Medicine
- Year
- 2024
- DOI
- 10.1111/jcmm.70236
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Myocardial Ischemia-Reperfusion Injury
- Body System
- Cardiovascular
TL;DR
Hydrogen gas (H2) treatment can reduce heart damage caused by interrupted and then restored blood flow, and this protective effect depends on a specific protein called PGC-1α.
Key Finding
Hydrogen gas protected rat heart tissue from ischemia-reperfusion injury by increasing PGC-1α expression, an effect that was largely lost when PGC-1α was deleted, indicating this protein is critical to hydrogen's cardioprotective mechanism.
Summary
Researchers used rat heart tissue to test whether hydrogen gas could protect against damage caused by temporarily cutting off blood flow and then restoring it (a condition called ischemia-reperfusion injury). They found that hydrogen gas increased levels of a protein called PGC-1α, which helps maintain healthy mitochondria (the energy-producing structures in cells). When hydrogen was applied, it reduced cell death, inflammation, and damage to heart tissue structure—but these protective effects largely disappeared when PGC-1α was removed, indicating this protein is essential for hydrogen's protective mechanism.
Practical Takeaway
This laboratory study in rat tissue suggests hydrogen gas may protect heart cells from damage related to blood flow interruption, but the findings are preliminary and from animal models only. Human studies would be needed to determine whether these protective effects translate to people, and the study does not address how hydrogen water (the form most consumers use) might compare to hydrogen gas.
Abstract
To investigate the application of H2 to alleviate cardiac ischaemia-reperfusion (I/R) injury in a PGC-1α-dependent manner. A rat in vitro myocardial I/R injury model was used, Western blot was used to detect the expression levels of apoptosis markers (Bax, cleaved caspase-3, Bcl2), inflammatory factors (IL-1β, TNF-α), mitochondrial fission (DRP1, MFF) and mitochondrial fusion (MFN1, MFN2, OPA1). HE staining was used to observe the effect of H2 on the myocardial tissue structure injured by I/R. Transmission electron microscopy (TEM) was used to observe the changes in the mitochondrial structure of myocardial tissue after I/R injury. Real-time quantitative PCR (qPCR) was used to detect the expression of PGC-1α in the myocardial tissue of rats after I/R injury and H2 treatment. H2 increases the expression level of PGC-1α, while the deletion of PGC-1α inhibited the therapeutic effect of H2. H2 can improve the changes of the myocardial tissue and mitochondrial structure caused by I/R injury. H2 treatment effectively inhibited the inflammatory response, and the loss of PGC-1α could inhibit the therapeutic effect of H2. The application of H2 can alleviate myocardial I/R injury, and the loss of PGC-1α weakens the protective effect of H2 on the I/R heart.