Hydrogen Gas Protects Lungs from Salt Water Damage in Animal Study
- Authors
- Mengyuan Diao, Sheng Zhang, Lifeng Wu, Le Huan, Fenglou Huang, Yunliang Cui, Zhaofen Lin
- Journal
- Inflammation
- Year
- 2016
- DOI
- 10.1007/s10753-016-0440-1
- Study Type
- Rabbit
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Lung Injury
- Body System
- Respiratory
TL;DR
Breathing in hydrogen gas can help reduce lung damage and improve healing after lungs are injured by seawater.
Key Finding
Inhaling 2% hydrogen gas significantly reduced lung damage and inflammation in rabbits with seawater-induced acute lung injury, with protective effects linked to activation of the Nrf2 antioxidant pathway.
Summary
Researchers exposed rabbits to seawater in their lungs to simulate acute lung injury, then tested whether inhaling hydrogen gas could help. Hydrogen gas inhalation reduced lung damage, decreased inflammatory markers (chemical messengers that trigger swelling and immune responses), and activated protective antioxidant pathways in the lungs. The study suggests hydrogen may work by boosting the body's natural defense systems against oxidative stress (cellular damage from unstable molecules).
Practical Takeaway
This animal study provides early evidence that hydrogen gas inhalation may help protect lungs from acute injury, but results from rabbits do not directly translate to humans. Much more research, including human trials, would be needed before any clinical recommendations could be made. The study's findings are promising for future investigation but should not be considered applicable to human treatment at this stage.
Abstract
Seawater instillation-induced acute lung injury involves oxidative stress and apoptosis. Although hydrogen gas inhalation is reportedly protective in multiple types of lung injury, the effect of hydrogen gas inhalation on seawater instillation-induced acute lung injury remains unknown. This study investigated the effect of hydrogen gas on seawater instillation-induced acute lung injury and explored the mechanisms involved. Rabbits were randomly assigned to control, hydrogen (2 % hydrogen gas inhalation), seawater (3 mL/kg seawater instillation), and seawater + hydrogen (3 mL/kg seawater instillation + 2 % hydrogen gas inhalation) groups. Arterial partial oxygen pressure and lung wet/dry weight ratio were detected. Protein content in bronchoalveolar lavage fluid (BALF) and serum as well as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were determined. Hematoxylin-eosin staining was used to monitor changes in lung specimens, and malondialdehyde (MDA) content and myeloperoxidase (MPO) activity were assayed. In addition, NF-E2-related factor (Nrf) 2 and heme oxygenase (HO)-1 mRNA and protein expression were measured, and apoptosis was assessed by measuring caspase-3 expression and using terminal deoxy-nucleotidyl transferase dUTP nick end-labeling (TUNEL) staining. Hydrogen gas inhalation markedly improved lung endothelial permeability and decreased both MDA content and MPO activity in lung tissue; these changes were associated with decreases in TNF-α, IL-1β, and IL-6 in BALF. Hydrogen gas also alleviated histopathological changes and cell apoptosis. Moreover, Nrf2 and HO-1 expressions were significantly activated and caspase-3 expression was inhibited. These results demonstrate that hydrogen gas inhalation attenuates seawater instillation-induced acute lung injury in rabbits and that the protective effects observed may be related to the activation of the Nrf2 pathway.