Hydrogen Protects Lung Cells from Oxygen Damage in Lab Study
- Authors
- Dan Wu, Mulin Liang, Hongxing Dang, Fang Fang, Feng Xu, Chengjun Liu
- Journal
- Biochemical and Biophysical Research Communications
- Year
- 2018
- DOI
- 10.1016/j.bbrc.2017.11.193
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Bronchopulmonary Dysplasia
- Body System
- Respiratory
TL;DR
Hydrogen gas can protect lung cells from damage caused by too much oxygen by influencing certain cell survival pathways.
Key Finding
Hydrogen prevented lung cell death from high oxygen exposure by activating a protective cellular pathway (PI3K/Akt/FoxO3a) that reduces pro-death signals and increases pro-survival signals.
Summary
This laboratory study examined how hydrogen protects lung cells from damage caused by high oxygen levels. Researchers exposed type II alveolar epithelial cells (cells that line the air sacs in lungs) to very high oxygen concentrations, which caused cell death. When hydrogen was added, it prevented this damage by activating a specific cellular pathway (PI3K/Akt/FoxO3a) that controls whether cells live or die. The protective effect disappeared when researchers blocked this pathway, showing that hydrogen works specifically through this mechanism.
Practical Takeaway
This is an early-stage laboratory study in isolated cells, not humans or animals, so its relevance to actual health outcomes remains unclear. The findings suggest a potential mechanism by which hydrogen might protect against oxygen-related lung injury, but much more research—including animal and human studies—would be needed to determine if this translates to clinical benefit for conditions like bronchopulmonary dysplasia.
Abstract
Oxidative stress is regarded as a key regulator in the pathogenesis of prolonged hyperoxia-induced lung injury, which causes injury to alveolar epithelial cells and eventually leads to development of bronchopulmonary dysplasia (BPD). Many studies have shown that hydrogen has a protective effect in a variety of cells. However, the mechanisms by which hydrogen rescues cells from damage due to oxidative stress in BPD remains to be fully elucidated. This study sought to evaluate the effects of hydrogen on hyperoxia-induced lung injury and to investigate the underlying mechanism. Primary type II alveolar epithelial cells (AECIIs) were divided into four groups: control (21% oxygen), hyperoxia (95% oxygen), hyperoxia + hydrogen, and hyperoxia + hydrogen + LY294002 (a PI3K/Akt inhibitor). Proliferation and apoptosis of AECIIs were assessed using MTS assay and flow cytometry (FCM), respectively. Gene and protein expression were detected by quantitative polymerase chain reaction (q-PCR) and western blot analysis. Stimulation with hyperoxia decreased the expression of P-Akt, P- FoxO3a, cyclinD1 and Bcl-2. Hyperoxic conditions increased levels of Bim, Bax, and Foxo3a, which induced proliferation restriction and apoptosis of AECIIs. These effects of hyperoxia were reversed with hydrogen pretreatment. Furthermore, the protective effects of hydrogen were abrogated by PI3K/Akt inhibitor LY294002. The results indicate that hydrogen protects AECIIs from hyperoxia-induced apoptosis by inhibiting apoptosis factors and promoting the expression of anti-apoptosis factors. These effects were associated with activation of the PI3K/Akt/FoxO3a pathway.