Hydrogen Gas Protects Lungs from Oxygen Damage in Rats
- Authors
- Qiang Sun, Wenjie Han, Huijun Hu, Danfeng Fan, Yanbo Li, Yu Zhang, Yan Lv, Mingxin Li, Shu-Yi Pan
- Journal
- Free Radical Research
- Year
- 2017
- DOI
- 10.1080/10715762.2017.1351027
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Hyperoxic Acute Lung Injury
- Body System
- Respiratory
TL;DR
Hydrogen treatment can significantly lessen lung damage caused by breathing pure oxygen by affecting certain protective processes in cells.
Key Finding
Hydrogen gas significantly reduced lung damage from prolonged oxygen exposure in rats by activating a protein called SIRT1, which reduced cellular stress and cell death.
Summary
This rat study investigated how hydrogen gas protects lungs from damage caused by prolonged exposure to pure oxygen. Researchers exposed rats to pure oxygen for 60 hours with or without hydrogen treatment, then measured lung damage, cell death, and stress markers inside cells. Hydrogen treatment reduced lung fluid buildup, cell death, and a type of cellular stress called endoplasmic reticulum stress, and this protection appeared to work through a protein called SIRT1.
Practical Takeaway
This is an early-stage rat study showing a potential mechanism for how hydrogen might protect against oxygen toxicity. However, this research has not been tested in humans, and the study does not tell us whether hydrogen water (the form most consumers use) would have similar effects. Much more research is needed before any clinical recommendations can be made.
Abstract
Hyperoxic acute lung injury (HALI) is a major clinical problem for patients undergoing supplemental oxygen therapy. Currently in clinical settings there exist no effective means of prevention or treatment methods. Our previous study found that: hydrogen could reduce HALI, as well as oxidative stress. This research will further explore the mechanism underlying the protective effect of hydrogen on oxygen toxicity. Rats were randomly assigned into three experimental groups and be exposed in oxygen chamber for 60 continuous hours:100% balanced air (control);100% oxygen (HALI);100% oxygen with hydrogen treatment (HALI+HRS). We examined lung function by wet to dry ratio of lung, lung pleural effusion and cell apoptosis. We also detected endoplasmic reticulum stress (ERS) by examining the expression of CHOP, GRP78 and XBP1. We further investigated the role of Sirtuin 1 (SIRT1) in HALI, which contributes to cellular regulation including ERS, by examining its expression after hydrogen treatment by applying SIRT1 inhibitor. Hydrogen could significantly reduce HALI by reducing lung edema and apoptosis, inhibiting the elevating of ERS and increased SIRT1 expression. By inhibition of SIRT1 expression, the effect of hydrogen on prevention of HALI is significantly weakened, the inhibition of the ERS was also reversed. Our findings indicate that hydrogen could reduce HALI related ERS, and the mechanism of hydrogen may be associated with upregulation of SIRT1, this study reveals the molecular mechanisms underlying the protective effect of hydrogen, which provides a new theoretical basis for clinical application of hydrogen.