Hydrogen Gas Helps Sleep Apnea Brain Problems in Rats

Authors
Journal
Brain Research Bulletin
Year
DOI
10.1016/j.brainresbull.2018.09.012
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Obstructive Sleep Apnea
Body System
Nervous System

TL;DR

Breathing hydrogen gas can help improve memory and brain function in rats that have a sleep disorder similar to sleep apnea.

Key Finding

Hydrogen gas inhalation improved memory and learning problems in rats exposed to chronic low-oxygen conditions, apparently by reducing oxidative stress and preventing brain cell death.

Summary

This study tested whether breathing hydrogen gas could help rats recover from memory and thinking problems caused by sleep apnea-like conditions (repeated drops in oxygen while sleeping). Rats exposed to low oxygen for 5 weeks showed memory problems, but those also given hydrogen gas for 2 hours daily performed better on memory tests. The researchers found that hydrogen reduced harmful molecules called oxidative stress in the brain and prevented brain cell death in the memory center (hippocampus).

Practical Takeaway

This early animal study suggests hydrogen gas may have protective effects on the brain during low-oxygen stress, but these results are from rats only and have not been tested in humans. Much more research would be needed before hydrogen could be considered a treatment for sleep apnea or related cognitive problems in people.

Abstract

Obstructive sleep apnea (OSA) is a very common breathing and sleep disorder characterized by intermittent hypoxia (IH), which is often associated with behavioral and neurocognitive functions impairment. Hydrogen (H2), as a novel and effective antioxidant, is reported to be a potential neuroprotective agent. The aim of this study is to investigate whether H2 could improve CIH-induced neurocognitive impairment and the related mechanism. Rats were exposed to IH for 5 weeks (8 h/day) and/or inhalation of H2 gas 2 h/day. Morris Water Maze test was used to appraise the spatial reference and working memory. The oxidative stress was evaluated through the level of MDA and SOD and apoptosis of hippocampal neurons was assayed with Bcl-2/Bax ratio and TUNEL staining. Our results showed that H2 treatment improved the CIH-induced spatial learning and memory impairments. Moreover, inhalation of H2 gas reduced the level of MDA and increased in the activity of SOD, indicating suppressed CIH-induced oxidative stress. In addition, H2 could increase expression of Bcl-2/Bax ratio and inhibited neurons apoptosis in hippocampus. In conclusion, these results suggest that inhalation of H2 could attenuate the CIH-induced neurocognitive functions impairment via anti-oxidant and anti-apoptosis effect. Additional, our findings may provide a potential therapeutic for neurocognitive diseases in patients with OSA.