Hydrogen Therapy Protects Newborn Lungs from Oxygen Damage
- Authors
- Mulin Liang, Feifei Song, Jin Wang, Chunli Yang, Huixi Yin, Wei Zhou
- Journal
- Frontiers in Pediatrics
- Year
- 2025
- DOI
- 10.3389/fped.2025.1662922
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Bronchopulmonary Dysplasia
- Body System
- Respiratory
TL;DR
Hydrogen protected developing lungs from oxygen-related injury by reducing cell death and activating protective cellular stress-response pathways.
Key Finding
Hydrogen treatment reduced lung damage and cell death in newborn rats with hyperoxia-induced bronchopulmonary dysplasia by activating a cellular pathway involving the aryl hydrocarbon receptor and its downstream target CPEB4.
Summary
This study examined how hydrogen gas might help treat bronchopulmonary dysplasia (BPD), a lung condition that affects premature infants exposed to high oxygen levels. Using newborn rats and lung cells in the lab, researchers found that hydrogen treatment reduced lung damage, prevented cell death, and improved the production of proteins needed for healthy lungs. The protective effect appeared to work through a specific cellular pathway involving a protein called the aryl hydrocarbon receptor.
Practical Takeaway
While these findings are promising, this research was conducted only in animals and laboratory cells—not in human infants. Early evidence suggests hydrogen may help protect developing lungs from oxygen-related injury through a specific cellular mechanism, but much more research, including human studies, would be needed before hydrogen could be considered a treatment for BPD in premature infants.
Abstract
Introduction: This study investigates the role and underlying mechanism of hydrogen (H₂) in hyperoxia-induced bronchopulmonary dysplasia (BPD), aiming to provide a theoretical foundation for developing effective BPD treatment strategies. Methods: A hyperoxia-induced BPD rat model and a rat type II alveolar epithelial cell (RLE-6TN) injury model were established. H₂ was administered to assess its effects on BPD rats, while hydrogen-rich medium was used to treat RLE-6TN cells to evaluate cell viability. In vivo and in vitro experiments were conducted to explore the regulatory influence of H₂ on the aryl hydrocarbon receptor (AHR). Additionally, AHR knockdown and overexpression experiments were performed to determine the impact of AHR on cell viability. Results: H₂ treatment ameliorated lung tissue pathology in BPD rats, reduced cellular apoptosis, enhanced the expression of surfactant proteins SP-A and SP-B, and modulated AHR and its downstream effector CPEB4, thereby alleviating endoplasmic reticulum (ER) stress. IN vitro, hydrogen-rich medium mitigated RLE-6TN cell injury, promoted AHR nuclear translocation, and activated CPEB4 expression. AHR overexpression enhanced RLE-6TN cell viability and exhibited strong binding affinity to the CPEB4 promoter. Discussion: H₂ alleviates ER stress and reduces apoptosis by regulating AHR and its downstream molecule CPEB4, thereby mitigating hyperoxia-induced BPD. The protective mechanism of H₂ may be closely associated with the modulation of the AHR-CPEB4 signaling pathway and the attenuation of ER stress.