Hydrogen Protects Lung Cells from Oxygen Toxicity in Lab Study
- Authors
- Xue Lu, Chao Wang, Dan Wu, Chao Zhang, Changxue Xiao, Feng Xu
- Journal
- Experimental Lung Research
- Year
- 2018
- DOI
- 10.1080/01902148.2019.1601296
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Hyperoxia-induced lung injury
- Body System
- Respiratory
TL;DR
Molecular hydrogen helps protect lung cells from damage caused by high levels of oxygen by influencing various proteins and biological processes.
Key Finding
Molecular hydrogen protected lung cells from damage caused by excessive oxygen exposure by reducing cell death, improving cell survival, and preserving cell function through multiple protective mechanisms.
Summary
Researchers exposed lung cells to very high oxygen levels (which damages them) and tested whether molecular hydrogen could protect them. They found that hydrogen-treated cells survived better, showed less cell death, and maintained better function compared to cells exposed to high oxygen alone. The study identified multiple proteins and biological pathways that appear to explain how hydrogen provides this protective effect.
Practical Takeaway
This laboratory study in isolated lung cells suggests hydrogen may have protective effects against oxygen-related lung injury, but it is a cell-culture study only—not tested in animals or humans. Much more research would be needed before any conclusions could be drawn about hydrogen's potential therapeutic use for lung conditions in people.
Abstract
Purpose/Aim: Exposure to hyperoxia leads to lung injury both in vivo and in vitro, molecular hydrogen has been reported to protect against hyperoxia-induced lung injury; however, the underlying molecular mechanisms remain largely unknown. The objective of this study was to characterize differentially regulated proteins and biological processes in hydrogen-treated hyperoxic primary type II alveolar epithelial cells (AECIIs) to elucidate the protective mechanism of hydrogen using quantitative proteomics. Materials and Methods: AECIIs were divided into three groups that were cultured for 24 h in three different conditions: control (21% oxygen), hyperoxia (95% oxygen), and hyperoxia + hydrogen. Morphologic examination, flow cytometric analysis, cell viability assessment and analysis of the expression of apoptosis-associated proteins Bax and Bcl-2 as well as AECI markers (AQP5, T1α) and an AECII marker (SP-C) were performed for each group. The TMT labeling quantitative proteome technique was used to detect changes in the protein expression profile, and bioinformatics analysis was performed. Results: Hydrogen plays a protective role in hyperoxia-induced damage in AECIIs, as evidenced by reduced apoptosis, increased viability and survival, improved morphology, and enhanced transdifferentiation of AECIIs into AECIs. A total of 5782 proteins were identified in our study, of which 162 were significantly altered in abundance after hyperoxia exposure, and 97 were significantly altered in abundance in response to hydrogen treatment. The Gene Ontology and KEGG enrichment analyses identified a large number of proteins and biological processes that may responsible for the protective effect of hydrogen, including VEGFA, PDGFB, IGFBP3, EDN1, NADPH oxidase, the coagulation cascade, etc. Conclusions: Molecular hydrogen protects AECIIs from hyperoxic injury by complex mechanisms involving a variety of proteins and biological processes, such as VEGFA, PDGFB, IGFBP3, EDN1, NADPH oxidase and the coagulation cascade. These findings suggest novel pathways that need to be investigated as possible therapeutic targets for hyperoxia-induced lung injury.