Hydrogen Gas Protects Heart Function During Sepsis in Mice
- Authors
- Yuanyuan Zhang, Aili Dong, Keliang Xie, Yong-Hao Yu
- Journal
- BioMed Research International
- Year
- 2020
- DOI
- 10.1155/2020/1568209
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Cardiovascular
TL;DR
Hydrogen gas treatment improves the health of cell powerhouses (mitochondria) and reduces organ damage during severe infection in mice, but this benefit is lost if a specific protective gene is missing.
Key Finding
Hydrogen gas protected heart mitochondria in septic mice, but this protection required two specific proteins (Nrf2 and HO-1) to work—when either was absent or blocked, hydrogen provided no benefit.
Summary
This study, which has been retracted, investigated how hydrogen gas affects heart cell function in mice with severe sepsis (a life-threatening infection). Researchers found that hydrogen gas treatment improved mitochondrial function (the energy-producing structures in cells) in heart tissue, but only when a specific protein called Nrf2 was present. When they blocked a related protein called HO-1, hydrogen's protective effects disappeared.
Practical Takeaway
This is an animal-only study that has been retracted, meaning the scientific community found significant issues with it. While it suggests hydrogen gas might theoretically help protect heart function during severe infection, the retraction means these findings cannot be relied upon and require independent validation before any conclusions can be drawn for human health.
Abstract
Enhancement of mitochondrial physiological function prevents sepsis‐induced dysfunction. The present study aimed to elucidate the mechanism by which hydrogen (H 2 ) affects mitochondrial function in a wild‐type (WT) and homozygous nuclear factor erythroid 2‐related factor 2 (Nrf2) knockout (KO, Nrf2 −/− ) murine model of sepsis. In myocardial tissues with severe sepsis, H 2 gas treatment reduced mitochondrial dysfunction, whereas zinc protoporphyrin (ZnPPIX) negated these beneficial effects. H 2 treatment upregulated the protein expression of mitofusin‐2 (Mfn2), peroxisome proliferator‐activated receptor‐gamma coactivator‐1 α (PGC‐1 α ), and protein heme oxygenase‐1 (HO‐1) in WT mice with severe sepsis but not in their Nrf2 −/− counterparts, and this upregulation was inhibited in the presence of ZnPPIX. In conclusion, the mechanism by which H 2 limits organ damage in mice with severe sepsis involves HO‐1, whereas the mechanism that limits severe sepsis‐related mitochondrial dysfunction involves both HO‐1 and Nrf2.