Hydrogen Water Protects Heart Cells from Damage After Heart Attack

Authors
Journal
ESC Heart Failure
Year
DOI
10.1002/ehf2.14492
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Myocardial Infarction
Body System
Cardiovascular

TL;DR

Hydrogen-rich saline (HRS) helps protect the heart from damage caused by interrupted blood flow and oxygen by targeting a specific microRNA and its associated protein.

Key Finding

Hydrogen-rich saline protected heart cells from damage by increasing miR-124-3p levels, which suppressed calpain1 activity and prevented cell death in laboratory and animal models of heart injury.

Summary

Researchers used mice and rat heart cells to study how hydrogen-rich saline (a salt solution containing dissolved hydrogen) protects heart tissue from damage caused by interrupted blood flow and oxygen loss. They found that hydrogen-rich saline works by increasing levels of a molecule called miR-124-3p, which then reduces activity of a protein called calpain1, ultimately preventing heart cells from dying and preserving their function.

Practical Takeaway

This early laboratory and animal study suggests hydrogen-rich saline may protect heart tissue through a specific molecular mechanism, but these findings have not been tested in humans. Much more research, including human trials, would be needed before any conclusions could be drawn about potential benefits for heart health in people.

Abstract

Aims: Molecular hydrogen has been exhibited a protective function in heart diseases. Our previous study demonstrated that hydrogen-rich saline (HRS) could scavenge free radicals selectively and alleviate the inflammatory response in the myocardial ischaemia/reperfusion (I/R) injury, but the underlying mechanism has not been fully clarified. Methods and results: Adult (10 weeks) C57BL/6 male mice and neonatal rat cardiomyocytes were used to establish I/R and hypoxia/reoxygenation (H/R) injury models. I/R and H/R models were treated with HRS to classify the mechanisms of cardioproctective function. In this study, we found that miR-124-3p was significantly decreased in both I/R and H/R models, while it was partially ameliorated by HRS pretreatment. HRS treatment also alleviated ischaemia-induced apoptotic cell death and increased cell viability during I/R process, whereas silencing expression of miR-124-3p abolished this protective effect. In addition, we identified calpain1 as a direct target of miR-124-3p, and up-regulation of miR-124-3 produced both activity and expression of calpain1. It was also found that compared with the HRS group, overexpression of calpain1 increased caspase-3 activities, promoted cleaved-caspase3 and Bax protein expressions, and correspondingly decreased Bcl-2, further reducing cell viability. These results illustrated that calpain1 overexpression attenuated protective effect of HRS on cardiomyocytes in H/R model. Conclusions: The present study showed a protective effect of HRS on I/R injury, which may be associated with miR-124-3p-calpain1 signalling pathway.