Hydrogen Gas Reduces Inflammation in Immune Cells
- Authors
- Hong-Guang Chen, Ke-Liang Xie, Huan-Zhi Han, Wei-Na Wang, Da-Quan Liu, Guo-Lin Wang, Yong-Hao Yu
- Journal
- International Journal of Surgery
- Year
- 2013
- DOI
- 10.1016/j.ijsu.2013.10.007
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Inflammation
- Body System
- Immune System
TL;DR
Breathing in molecular hydrogen gas can help reduce inflammation in immune cells by activating a protective protein.
Key Finding
Molecular hydrogen reduced pro-inflammatory molecules and increased anti-inflammatory molecules in activated immune cells, with this effect partly dependent on activation of a protein called heme oxygenase-1.
Summary
This laboratory study tested whether molecular hydrogen (H2) could reduce inflammation in immune cells called macrophages that were activated by a bacterial toxin. Researchers found that hydrogen gas reduced inflammatory molecules (TNF-α, IL-1β, HMGB1) while increasing an anti-inflammatory molecule (IL-10). The effect appeared to work through a protein called heme oxygenase-1 (HO-1), since blocking this protein partially reversed hydrogen's benefits.
Practical Takeaway
This is an early-stage cell culture study showing hydrogen may have anti-inflammatory potential, but it was conducted only in laboratory cells, not in animals or humans. Much more research would be needed to determine whether these effects translate to health benefits in people.
Abstract
Background: Molecular hydrogen (H2) as a new medical gas has an anti-inflammatory effect. In the present study, we investigated whether heme oxygenase-1 (HO-1) contributes to the anti-inflammatory effect of H2 in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Methods: RAW 264.7 macrophages were stimulated by LPS (1 μg/mL) with presence or absence of different concentrations of H2. Cell viability and injury were tested by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay and lactate dehydrogenase (LDH) release, respectively. The cell culture supernatants were collected to measure inflammatory cytokines [TNF-α, IL-1β, HMGB1 (high mobility group box-1) and IL-10] at different time points. Moreover, HO-1 protein expression and activity were tested at different time points. In addition, to further identify the role of HO-1 in this process, zinc protoporphyrin (ZnPP)-IX, an HO-1 inhibitor, was used. Results: H2 treatment had no significant influence on cell viability and injury in normally cultured RAW 264.7 macrophages. Moreover, H₂ treatment dose-dependently attenuated the increased levels of pro-inflammatory cytokines (TNF-α, IL-1β, HMGB1), but further increased the level of anti-inflammatory cytokine IL-10 at 3 h, 6 h, 12 h and 24 h after LPS stimulation. Furthermore, H₂ treatment could also dose-dependently increase the HO-1 protein expression and activity at 3 h, 6 h, 12 h and 24 h in LPS-activated macrophages. In addition, blockade of HO-1 activity with ZnPP-IX partly reversed the anti-inflammatory effect of H₂ in LPS-stimulated macrophages. Conclusions: Molecular hydrogen exerts a regulating role in the release of pro- and anti-inflammatory cytokines in LPS-stimulated macrophages, and this effect is at least partly mediated by HO-1 expression and activation.