Hydrogen Gas Protects Lungs from Sepsis Damage in Mice Study
- Authors
- Yang Yu, Yongyan Yang, Man Yang, Chunyan Wang, Keliang Xie, Yong-Hao Yu
- Journal
- International Immunopharmacology
- Year
- 2019
- DOI
- 10.1016/j.intimp.2019.01.022
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Respiratory
TL;DR
Breathing in 2% hydrogen gas helps mice survive and reduces lung damage from sepsis by affecting certain protective and harmful molecules, but this benefit depends on a specific gene called Nrf2.
Key Finding
Hydrogen gas inhalation improved survival rates and reduced lung injury in septic mice by activating a protein called Nrf2, which then boosted antioxidant defenses and reduced harmful inflammatory molecules.
Summary
Researchers tested whether inhaling hydrogen gas could protect the lungs of mice with sepsis (a life-threatening infection). They found that mice receiving hydrogen gas treatment had better survival rates, less lung swelling, and lower levels of harmful inflammatory molecules. The protective effect depended on a specific protein called Nrf2, which hydrogen gas activated to trigger the body's natural defense systems.
Practical Takeaway
This is an early-stage animal study showing hydrogen gas may help protect lungs during severe infection, but results from mouse models do not automatically translate to humans. Much more research, including human trials, would be needed before hydrogen gas could be considered a sepsis treatment. The study's reliance on a specific molecular pathway (Nrf2) also suggests effects may vary between individuals.
Abstract
Background: Lung injury is a vital contributor of mortality in septic patients. Our previous studies have found that molecular hydrogen (H2), which has anti-oxidant, anti-inflammatory, and anti-apoptosis effects, had a therapeutic effect on a septic animal model through increasing expression of nuclear factor-erythroid 2-related factor 2 (Nrf2). The aim of this research was to investigate the effects of 2% H2 gas inhalation on sepsis-induced lung injury and its underlying mechanisms. Methods: Male wild-type (WT) and Nrf2-knockout (Nrf2-KO) ICR mice underwent sham or cecal ligation and puncture (CLP) operation. Two percent of H2 gas was inhaled for 60 min beginning at both 1 h and 6 h after sham or CLP surgery. To assess the severity of septic lung injury, the 7-day survival rate, wet/dry (W/D) weight ratio of lung tissue, lung histopathologic score, pro-inflammatory cytokines (tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), high-mobility group box 1 (HMGB1)), anti-inflammatory cytokine (interleukin 10 (IL-10)), antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and heme oxygenase 1 (HO-1)), and an oxidative product (malondialdehyde (MDA)) were detected after sham or CLP operation. The histopathologic changes were observed in lung tissues by hematoxylin and eosin (HE) staining, and pro-inflammatory cytokines (TNF-α and IL-6), anti-inflammatory cytokine (IL-10), antioxidant enzymes (SOD and CAT), and MDA were detected in lung tissues by an enzyme-linked immunosorbent assay (ELISA). Results: The results indicated that 2% H2 gas treatment increased the survival rates, decreased the W/D weight ratio and the lung injury score, alleviated the injuries caused by oxidative stress and inflammation, and induced HO-1 level but reduced HMGB1 level in WT but not Krf2-KO mice. These data reveal that H2 gas could suppress lung injury in septic mice through regulation of HO-1 and HMGB1 expression and that Nrf2 plays a main role in the protective effects of H2 gas on lung damage caused by sepsis.