Hydrogen Boosts Lung Medicine Effectiveness in Silicosis Treatment
- Authors
- Kang Xiao, Ming Li, Yingwen Mu, Yuxin Sun, Sirui Wang, Shangya Chen, Jiazi Ma, Mao Cao, Yong Yang, Hua Shao, Xuansheng Ding, Guanqun Cui, Zhongjun Du
- Journal
- Frontiers in Bioengineering and Biotechnology
- Year
- 2026
- DOI
- 10.3389/fbioe.2025.1668524
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Silicosis
- Body System
- Respiratory
TL;DR
Hydrogen inhalation improved lung damage in silicosis and increased delivery of therapeutic drugs to lung tissue by reducing oxidative stress and vascular dysfunction.
Key Finding
In mice with silicosis, inhaling hydrogen gas alongside tetrandrine treatment increased the drug's concentration in lung tissue by 60% (from 50 to 80 ng/mg) and improved disease severity by reducing oxidative stress and blood vessel dysfunction.
Summary
Silicosis is a serious lung disease caused by inhaling dust, and while a drug called tetrandrine is used to treat it in China, it doesn't work well because the drug doesn't reach high enough levels in lung tissue. In this mouse study, researchers found that when hydrogen gas was added to tetrandrine treatment, it reduced oxidative stress (harmful chemical reactions in cells) and improved how well blood vessels in the lungs functioned, which allowed more of the drug to reach the lung tissue and work better.
Practical Takeaway
This early-stage mouse study suggests hydrogen gas inhalation may help tetrandrine work more effectively for silicosis by improving how the drug reaches lung tissue. However, this is preliminary research in animals only, and much more work—including human studies—would be needed before hydrogen could be recommended as a silicosis treatment. People with silicosis should continue following their doctor's current treatment plans.
Abstract
Objective: Silicosis, a lung disease associated with occupational exposure. Tetrandrine has been approved for the treatment of silicosis in China, but it still cannot be cured. This study aims to investigate the reasons behind the low concentration of tetrandrine (Tet) in lung tissue and propose a treatment plan. Methods: We first established a silicosis mouse and employed a combination of histological examination, Western blot analysis, immunofluorescence, and single-cell RNA sequencing to clarify the relationship between oxidative stress vascular endothelial mesenchymal transition (EndMT), and Tet concentration in lung tissue. Results: The study indicated that there is excessive activation of OS and EndMT in silicosis while concurrently reducing Tet concentration in lung tissue (from 94.8 ± 10.4 ng/mg to 54 ± 6.2 ng/mg). Furthermore, combined inhalation of hydrogen (H2) improved both the severity of silicosis and Tet concentration in lung tissue (from 50 ng/mg to 80 ng/mg). The proposed mechanism suggests that H2 inhibits the release of amyloid precursor protein (APP) in apoptotic alveolar macrophages. Additionally, the interaction between APP and CD74 in vascular endothelial cells was diminished, thereby inhibiting biological processes associated with endothelial mesenchymal transition, alleviating pulmonary vascular stenosis, and enhancing the concentration of therapeutic agents in lung tissue. Conclusion: Hydrogen can improve the tissue concentration of tetrandrine by anti-OS-induced EndMT.