Hydrogen Gas Speeds Up Wound Healing by Reducing Inflammation
- Authors
- Pengxiang Zhao, Zisong Cai, Xujuan Zhang, Mengyu Liu, Fei Xie, Ziyi Liu, Shidong Lu, Xuemei Ma
- Journal
- Pharmaceuticals
- Year
- 2023
- DOI
- 10.3390/ph16060885
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Skin Wounds
- Body System
- Integumentary
TL;DR
Breathing in molecular hydrogen (H2) gas can speed up the healing process by quickly turning certain immune cells from a pro-inflammatory to a healing-promoting type in mice with skin wounds.
Key Finding
Hydrogen gas inhalation accelerated the shift from inflammatory to healing-type macrophages by 2-3 days in mouse wound healing, without compromising the initial immune response.
Summary
Researchers studied how molecular hydrogen (a gas) affects wound healing in mice. They found that inhaling hydrogen gas sped up the conversion of immune cells called macrophages from an inflammatory type (M1) to a healing type (M2) by 2-3 days. This happened without interfering with the body's initial immune response, suggesting hydrogen may help wounds heal faster by reducing inflammation.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen gas may support faster wound healing by modulating immune responses. However, these results are from mice only, and human studies would be needed to determine if similar effects occur in people. The mechanism appears more complex than simple antioxidant activity, which may be important for future therapeutic development.
Abstract
The heterogeneous and highly plastic cell populations of macrophages are important mediators of cellular responses during all stages of wound healing, especially in the inflammatory stage. Molecular hydrogen (H2), which has potent antioxidant and anti-inflammatory effects, has been shown to promote M2 polarization in injury and disease. However, more in vivo time series studies of the role of M1-to-M2 polarization in wound healing are needed. In the current study, we performed time series experiments on a dorsal full-thickness skin defect mouse model in the inflammatory stage to examine the effects of H2 inhalation. Our results revealed that H2 could promote very early M1-to-M2 polarization (on days 2-3 post wounding, 2-3 days earlier than in conventional wound healing), without disturbing the functions of the M1 phenotype. Time series analysis of the transcriptome, blood cell counts, and multiple cytokines further indicated that peripheral blood monocytes were a source of H2-induced M2 macrophages and that the functions of H2 in macrophage polarization were not only dependent on its antioxidant effects. Therefore, we believe that H2 could reduce inflammation in wound care by shifting early macrophage polarization in clinical settings.