Hydrogen Gas Protects Lungs from Ventilator Damage in Mice Study
- Authors
- Chien-Sheng Huang, Tomohiro Kawamura, Ximei Peng, Naobumi Tochigi, Norihisa Shigemura, Timothy R. Billiar, Atsunori Nakao, Yoshiya Toyoda
- Journal
- Biochemical and Biophysical Research Communications
- Year
- 2011
- DOI
- 10.1016/j.bbrc.2011.04.008
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- United States
- Health Condition
- Ventilator-Induced Lung Injury
- Body System
- Respiratory
TL;DR
Breathing in hydrogen gas can help reduce lung damage caused by ventilators, possibly by affecting a specific cell-protecting pathway in the body.
Key Finding
Inhaled hydrogen gas reduced lung damage in mechanically ventilated mice by triggering early activation of a cellular defense pathway (NFκB) that increased protective proteins and decreased inflammatory damage.
Summary
This study used mice on mechanical ventilators to test whether breathing hydrogen gas could protect lung tissue from damage. Researchers found that hydrogen gas activated a cellular defense pathway (called NFκB) that increased protective proteins and reduced harmful inflammation and cell death in the lungs. The effect was reversed when they blocked this pathway, suggesting the NFκB activation was key to hydrogen's protective effects.
Practical Takeaway
This is early research in mice showing a potential mechanism for how hydrogen gas might protect lungs during mechanical ventilation. However, these findings have not been tested in humans yet, and the study does not demonstrate that hydrogen would be effective or safe as a clinical treatment. Much more research would be needed before any conclusions could be drawn about human applications.
Abstract
We recently demonstrated the inhalation of hydrogen gas, a novel medical therapeutic gas, ameliorates ventilator-induced lung injury (VILI); however, the molecular mechanisms by which hydrogen ameliorates VILI remain unclear. Therefore, we investigated whether inhaled hydrogen gas modulates the nuclear factor-kappa B (NFκB) signaling pathway. VILI was generated in male C57BL6 mice by performing a tracheostomy and placing the mice on a mechanical ventilator (tidal volume of 30 ml/kg or 10 ml/kg without positive end-expiratory pressure). The ventilator delivered either 2% nitrogen or 2% hydrogen in balanced air. NFκB activation, as indicated by NFκB DNA binding, was detected by electrophoretic mobility shift assays and enzyme-linked immunosorbent assay. Hydrogen gas inhalation increased NFκB DNA binding after 1h of ventilation and decreased NFκB DNA binding after 2h of ventilation, as compared with controls. The early activation of NFκB during hydrogen treatment was correlated with elevated levels of the antiapoptotic protein Bcl-2 and decreased levels of Bax. Hydrogen inhalation increased oxygen tension, decreased lung edema, and decreased the expression of proinflammatory mediators. Chemical inhibition of early NFκB activation using SN50 reversed these protective effects. NFκB activation and an associated increase in the expression of Bcl-2 may contribute, in part, to the cytoprotective effects of hydrogen against apoptotic and inflammatory signaling pathway activation during VILI.