Magnesium Helps Release Hydrogen to Protect Hearts from Failure
- Authors
- Fengbao Chen, Ruimin Chen, Lili Yang, Bowen Shen, Yunting Wang, Yongfeng Gao, Rui Tan, Xiaomin Zhao
- Journal
- Medical Gas Research
- Year
- 2024
- DOI
- 10.4103/mgr.MEDGASRES-D-24-00135
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Heart Failure
- Body System
- Cardiovascular
TL;DR
Magnesium helps protect the heart by releasing hydrogen, which reduces cell stress and death in heart failure.
Key Finding
Magnesium treatment improved cardiac function and reduced heart damage markers in rats with induced heart failure, while also increasing hydrogen levels in blood and heart tissue.
Summary
Researchers tested whether magnesium could help the body release hydrogen gas, which might protect heart tissue from damage. In rats with heart failure induced by a drug, magnesium treatment improved heart function, reduced markers of heart damage in the blood, and decreased harmful changes to heart tissue. The study also tested hydrogen-rich solutions on heart cells in a lab dish, which showed similar protective effects by reducing cell death and stress inside cells.
Practical Takeaway
This is an early-stage animal study that suggests magnesium-assisted hydrogen may have heart-protective properties by reducing cellular stress and cell death. However, these results are from rats and lab-grown cells, not humans, so it's unclear whether the effects would translate to people with heart failure. Much more research, including human trials, would be needed before any health recommendations could be made.
Abstract
Heart failure (HF) is a leading cause of mortality among patients with cardiovascular disease and is often associated with myocardial apoptosis and endoplasmic reticulum stress (ERS). While hydrogen has demonstrated potential in reducing oxidative stress and ERS, recent evidence suggests that magnesium may aid in hydrogen release within the body, further enhancing these protective effects. This study aimed to investigate the cardioprotective effects of magnesium in reducing apoptosis and ERS through hydrogen release in a rat model of isoproterenol (ISO)-induced HF. Magnesium was administered orally to ISO-induced HF rats, which improved cardiac function, reduced myocardial fibrosis and cardiac hypertrophy, and lowered the plasma levels of creatine kinase-MB, cardiac troponin-I, and N-terminal B-type natriuretic peptide precursor in ISO-induced HF rats. It also inhibited cardiomyocyte apoptosis by upregulating B-cell lymphoma-2, downregulating Bcl-2-associated X protein, and suppressing ERS markers (glucose-related protein 78, activating transcription factor 4, and C/EBP-homologous protein). Magnesium also elevated hydrogen levels in blood, plasma, and cardiac tissue, as well as in artificial gastric juice and pure water, where hydrogen release lasted for at least four hours. Additionally, complementary in vitro experiments were conducted using H9C2 cardiomyocyte injury models, with hydrogen-rich culture medium as the intervention. Hydrogen-rich culture medium improved the survival and proliferation of ISO-treated H9C2 cells, reduced the cell surface area, inhibited apoptosis, and downregulated ERS pathway proteins. However, the protective effects of hydrogen were negated by tunicamycin (an inducer of ERS) in H9C2 cells. In conclusion, magnesium exerts significant cardioprotection by mitigating ERS and apoptosis through hydrogen release effects in ISO-induced HF.