Hydrogen ameliorates chronic intermittent hypoxia-induced neurocognitive impairment via inhibiting oxidative stress.

Highlights • H 2 attenuated CIH-induced either spatial reference or working memory impairment. • H 2 inhalation significantly suppressed oxidative stress in hippocampal neurons. • H 2 inhibited CIH-induced hippocampal neuron apoptosis via Bcl-2/ Bax pathway. 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 (H 2), as a novel and effective antioxidant, is reported to be a potential neuroprotective agent. The aim of this study is to investigate whether H 2 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 H 2 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 H 2 treatment improved the CIH-induced spatial learning and memory impairments. Moreover, inhalation of H 2 gas reduced the level of MDA and increased in the activity of SOD, indicating suppressed CIH-induced oxidative stress. In addition, H 2 could increase expression of Bcl-2/Bax ratio and inhibited neurons apoptosis in hippocampus. In conclusion, these results suggest that inhalation of H 2 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. [ABSTRACT FROM AUTHOR]