Hydrogen Therapy Protects Lungs from Sepsis-Related Damage in Mice
- Authors
- Qian Li, Min Shi, Yang Ang, Pan Yu, Bing Wan, Bin Lin, Wei Chen, Zichuan Yue, Yadan Shi, Faqi Liu, Wang Hao, Manlin Duan, Yun Long, Hongguang Bao
- Journal
- Molecular Immunology
- Year
- 2024
- DOI
- 10.1016/j.molimm.2024.02.001
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Respiratory
TL;DR
Hydrogen treatment helps mice recover from severe lung damage caused by infection-related inflammation by activating a protective pathway in the body.
Key Finding
Hydrogen gas reduced lung injury and inflammation in mice exposed to bacterial toxins by activating the AMPK pathway, which suppressed inflammatory chemicals and regulated cell death proteins.
Summary
Researchers tested whether hydrogen gas could help treat acute lung injury (severe inflammation in the lungs) caused by bacterial toxins in mice and human lung cells. They found that hydrogen improved survival rates, prevented weight loss, restored lung function, and reduced inflammatory chemicals in the lungs by activating a cellular energy-sensing pathway called AMPK.
Practical Takeaway
This is early laboratory research in mice and cultured cells, not humans. While the results suggest hydrogen may have potential for treating sepsis-related lung injury through a specific cellular mechanism, much more research—including human studies—would be needed before any clinical applications could be considered.
Abstract
Septic lung injury is characterized by uncontrollable inflammatory infiltrations and acute onset bilateral hypoxemia. Evidence has emerged of the beneficial effect of hydrogen in acute lung injury (ALI), but the underlying mechanism is unclear. In this research, the recovery action of hydrogen on lipopolysaccharide (LPS)-induced ALI in mice and A549 cells was investigated. The 7-day survival rate and body weight of mice were measured after intraperitoneal injection of LPS. Lung function was determined by a whole body plethysmography (WBP) system using the indicators respiratory rate and enhanced pause. Hematoxylin and eosin (HE) staining confirmed the signs of pulmonary edema and inflammatory ooze. Reverse transcription-polymerase chain reaction (RT-PCR) quantification was used to detect the expression of inflammatory factors. Western blotting analysis evaluated the expression levels of involved proteins in the AMP-activated protein kinase (AMPK) pathway. The experimental results confirmed that hydrogen provided an essential solution to the dissipative effects of LPS on survival rate, weight loss and lung function. The LPS-stimulated inflammatory factors, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were also suppressed by hydrogen in A549 cells. Western blot analysis showed that hydrogen significantly upregulated the levels of phosphorylated AMPK (p-AMPK) and lowered the LPS-induced increased expression of dynamin-related protein 1 (Drp1) and Caspase3. These findings prove that hydrogen attenuated LPS-treated ALI by activating the AMPK pathway, supporting the feasibility of hydrogen treatment for sepsis. Keywords: AMPK; Acute lung injury; Caspase3; Drp1; Hydrogen; LPS.