Hydrogen Gas Protects Lungs After Brain Injury in Mice Study
- Authors
- Lingling Liu, Shuzhi Wang, Lianhao Jiang, Jiwei Wang, Jun Chen, Hongtao Zhang, Yuanlin Wang
- Journal
- BMC Chemistry
- Year
- 2025
- DOI
- 10.1186/s13065-025-01513-2
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Traumatic Brain Injury
- Body System
- Nervous System
TL;DR
Breathing in 2% hydrogen gas can reduce lung damage caused by traumatic brain injury (TBI) by calming inflammation.
Key Finding
Inhaling 2% hydrogen gas significantly reduced lung injury in mice with traumatic brain injury by suppressing NLRP3 inflammasome activation, a key driver of inflammation.
Summary
In mice with traumatic brain injury (TBI), researchers tested whether inhaling hydrogen gas could reduce lung damage that sometimes occurs after brain injury. They found that 2% hydrogen gas inhalation reduced lung injury by blocking a specific inflammatory pathway called NLRP3 inflammasome (a cellular alarm system that triggers inflammation). When hydrogen was combined with a drug that also blocks this pathway, the protective effect was even stronger.
Practical Takeaway
This mouse study suggests hydrogen gas may help prevent secondary lung complications after traumatic brain injury, but this is early-stage research. The findings would need to be tested in human trials before any therapeutic recommendations could be made. The study does not address whether these results would apply to humans or what the optimal dosing and timing might be.
Abstract
Introduction: Hydrogen gas has demonstrated significant antioxidant and anti-inflammatory properties, suggesting potential therapeutic benefits in TBI. Methods: We subjected to controlled cortical impact in mice to construct TBI model. They received an intraperitoneal injection of MCC950, a selective NLRP3 inhibitor, at 10 mg/kg 30 min before TBI. Inhalation of 2% H2 is adopted in TBI mice for 60 min, starting 1 and 6 h post-TBI. 24 h after H2 inhalation, we extracted tissues and analyzed injury related changes. The H2 levels in arterial and venous were tracked after inhalation. Lung tissue was examined for histopathological changes and apoptosis using H&E and TUNEL assays. The total protein in the BALF, oxygenation index, lung wet-to-dry weight ratio, and lung MPO activity were measured to evaluate the severity of TBI-induced lung injury. Protein and mRNA levels of NLRP3, ASC, Caspase-1, IL-18, and IL-1β in the lung tissue were quantified using western blotting and quantitative PCR. The expression changes and distribution status of NLRP3 and Caspase-1 were examined by immunofluorescence and immunohistochemistry staining. Results: Significant lung injury at 24 h post-TBI got significantly reduced by treatment of 2% H2. TBI activated the NLRP3 inflammasome, increasing NLRP3, ASC, and caspase-1 levels, to lead to higher IL-1β and IL-18 secretion in the lungs. Blocking NLRP3 reduced lung damage from TBI, and its combination with 2% H2 provided better protection than either treatment alone. Conclusions: 2% H2 can protect against TBI-induced lung injury by inhibiting NLRP3 inflammasome activation, thereby alleviating inflammation and inhibiting apoptosis.