Hydrogen Gas Helps Protect Heart from Damage in Rats

Authors
Journal
World Journal of Cardiology
Year
DOI
10.4330/wjc.v17.i6.104832
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Right Ventricular Hypertrophy
Body System
Cardiovascular

TL;DR

Breathing in hydrogen gas can reduce heart muscle thickening in rats by preventing a specific type of cell death related to iron and oxidative stress.

Key Finding

Hydrogen gas inhalation reduced right ventricular wall thickness and improved heart function in rats with induced heart chamber enlargement, working by blocking ferroptosis through activation of protective antioxidant pathways.

Summary

This study tested whether hydrogen gas could help treat right ventricular hypertrophy (enlargement of the heart's right chamber due to pressure overload) in rats. Researchers gave rats hydrogen gas to breathe for 21 days and found that the thickened heart wall became thinner and the heart's pumping ability improved. In lab-grown heart cells, hydrogen also reduced enlargement by blocking a type of cell death called ferroptosis (iron-dependent damage) and activating protective cellular pathways.

Practical Takeaway

This early-stage animal study suggests hydrogen gas may have potential for treating certain types of heart enlargement, but results from rat studies do not directly apply to humans. Much more research, including human trials, would be needed before hydrogen could be considered a treatment for heart conditions. The study's findings are preliminary and should not be interpreted as medical advice.

Abstract

Background: Right ventricular hypertrophy (RVH) occurs because of volume or pressure overload within the right ventricular (RV) system. RVH is associated with complex pathological changes, including myocardial cell injury, apoptosis, myocardial fibrosis, neuroendocrine disturbances, and abnormal water and liquid metabolism. Ferroptosis, a novel type of iron-dependent cell death characterized by lipid peroxide accumulation, is an important mechanism of cardiomyocyte death. However, the role of ferroptosis in RVH has rarely been studied. We hypothesize that hydrogen (H2), an experimental medical gas with superior distribution characteristics, inhibits ferroptosis. Aim: To explore the protective effect of H2 on RVH and the mechanism by which H2 regulates ferroptosis. Methods: An in vivo RVH rat model was induced by monocrotaline (MCT) in 30 male Sprague-Dawley rats. An H9C2 cell model was treated with angiotensin II to simulate pressure overload in the RV system in vitro. H2 was administered to rats by inhalation (2% for 3 hours daily for 21 days) and added to the cell culture medium. The Nrf2 inhibitor ML385 (1 μM) was used to investigate anti-ferroptotic mechanisms. Results: In MCT-treated rats, H2 inhalation decreased RVH; the RV wall thickness decreased from 3.5 ± 0.3 mm to 2.8 ± 0.2 mm (P < 0.05) and the RV ejection fraction increased from 45 ± 3% to 52 ± 4% (P < 0.05). In H9C2 cells, H2 alleviated hypertrophy. H2 inhibited ferroptosis by modulating the iron content, oxidative stress, and ferroptosis-related proteins, thereby restoring the Nrf2/HO-1 signaling pathway. Conclusion: H2 retards RVH by inhibiting ferroptosis via Nrf2/HO-1 restoration, suggesting a new treatment strategy.