Hydrogen Gas Dramatically Improves Stroke Survival in Mice Study

Authors
Journal
Shock
Year
DOI
10.1097/SHK.0b013e31824ed57c
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Stroke
Body System
Nervous System

TL;DR

Breathing hydrogen gas significantly increased survival and reduced brain damage in mice after a stroke caused by lack of blood flow to the brain.

Key Finding

Hydrogen gas treatment increased the 7-day survival rate of mice with global cerebral ischemia-reperfusion injury from 8.3% to 50%, while also reducing brain damage and swelling.

Summary

Researchers tested whether hydrogen gas could help mice survive a type of brain injury caused by temporarily cutting off blood flow to the brain. They found that mice treated with hydrogen gas had much higher survival rates (50%) compared to untreated mice (8.3%) seven days after the injury. The hydrogen gas appeared to work by reducing harmful molecules called free radicals that damage brain cells, and it also reduced brain swelling.

Practical Takeaway

This is an early-stage animal study showing hydrogen gas may help protect the brain after stroke-like injuries in mice. However, these results are from mice only and do not yet tell us whether hydrogen gas would be safe or effective in humans. Much more research, including human clinical trials, would be needed before any conclusions could be drawn about its potential use in stroke treatment.

Abstract

Global cerebral ischemia and reperfusion (I/R) often result in high mortality. Free radicals have been reported to play an important role in global cerebral I/R, and therefore, reduction of these might improve the outcome. Here, we investigated the effect of hydrogen gas (H2) (a strong free radical scavenger) on the survival rate of mice following global cerebral I/R. We further examined the histopathological outcome and also the brain water content (as a possible determinant of mortality). Male C57BL/6J mice were subjected to global cerebral I/R by means of 45-min bilateral common carotid artery occlusion (BCCAO). A total of 160 mice were divided into three groups: sham surgery (sham group), BCCAO without H2 (BCCAO group), and BCCAO treated with 1.3% H2 (BCCAO + H2 group). We observed that H2 treatment significantly (P = 0.0232) improved the 7-day survival rate of mice, from 8.3% (BCCAO group, n = 12) to 50% (BCCAO + H2 group, n = 10). Histopathological analysis revealed that H2 treatment significantly attenuated neuronal injury and autophagy in the hippocampal cornu ammonis 1 sector and also brain edema, after 24 h of reperfusion. The beneficial effects of H2 treatment on brain injury were associated with significantly lower levels of oxidative stress markers (8-hydroxy-2'-deoxyguanosine and malondialdehyde) in the brain tissue. Thus, we believe that H2 may be an effective treatment for global cerebral I/R.