Hydrogen Gas Protects Brain After Stroke in Mice Study
- Authors
- Anatol Manaenko, Tim Lekic, Qingyi Ma, Robert P. Ostrowski, John H. Zhang, Jiping Tang
- Journal
- Acta Neurochirurgica Supplementum
- Year
- 2011
- DOI
- 10.1007/978-3-7091-0693-8_30
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- United States
- Health Condition
- Intracerebral Hemorrhage
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas shortly after a brain hemorrhage can temporarily reduce brain swelling and improve brain function in mice.
Key Finding
Hydrogen inhalation reduced brain swelling and improved neurological function in mice 24 hours after brain injury, but the protective effect diminished significantly by 72 hours.
Summary
Researchers gave mice a brain injury similar to a stroke and tested whether breathing hydrogen gas could help protect their brains. Hydrogen gas can neutralize harmful molecules (called reactive oxygen species) that form after brain injury. The mice that breathed hydrogen showed less brain swelling and better neurological function 24 hours after injury, but these benefits largely disappeared by 72 hours.
Practical Takeaway
This early-stage mouse study suggests hydrogen gas may have acute protective effects immediately after brain injury, but the benefits appear temporary with a single treatment. Since this is only a mouse study and the effect didn't last beyond 24 hours, much more research—including human trials—would be needed before drawing any conclusions about hydrogen's usefulness for stroke or brain injury in people.
Abstract
Oxidative stress contributes significantly to the development of secondary brain injury after intracerebral hemorrhage (ICH). It has been previously demonstrated that hydrogen gas can decrease oxidative stress by scavenging reactive oxygen species. We hypothesized that hydrogen therapy will reduce brain oxidative stress in mice after ICH and thereby will lead to reduced brain edema and improved neurological outcomes. CD1 male mice (weight 30-35 g) were divided into the following groups: sham, ICH+vehicle (room air), ICH+1-h hydrogen treatment, and ICH+2-h hydrogen treatment. ICH was induced by injection of bacterial collagenase into the right basal ganglia. The evaluation of outcomes was done at two time points: 24 and 72 h post-ICH. Brain water content was measured for assessment of brain edema (wet/dry weight method), and three neurological tests were performed pre- and postoperatively. Collagenase injection was found to induce brain edema and impair functional performance of rats. The hydrogen inhalation reduced these effects acutely (24 h); however it exhibited only a tendency to improvement in the delayed study (72 h). Our results suggest that hydrogen inhalation exerts an acute brain-protective effect in the mouse ICH model. However, the acute hydrogen therapy alone is not sufficient to improve delayed ICH outcomes in this model.