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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]

Abstract Aims Hydrogen gas (H 2) has a diversity of effects such as anti-apoptotic, anti-inflammatory and anti-oxidative properties. However, molecular mechanism underlying the potential effect of H 2 on chronic intermittent hypoxia (CIH) induced renal injury remains obscure. Materials and methods In the present study, adult male Sprague-Dawley rats were randomly allocated into four groups: control (CON) group, CIH group, CIH with H 2 treatment (CIH + H 2) group, and control with H 2 treatment (CON + H 2) group. Oxidative stress, autophagy and endoplasmic reticulum (ER) stress were detected to determine how H 2 affected the renal function of CIH exposed rats. Key findings We demonstrated that rats who inhale hydrogen gas showed improved renal function, alleviated pathological damage, oxidative stress and apoptosis in CIH rats. Meanwhile, CIH-induced endoplasmic reticulum stress was decreased by H 2 as the expressions of CHOP, caspase-12, and GRP78 were down-regulated. Furthermore, relative higher levels of LC3-II/I ratio and Beclin-1, with decreased expression of p62, were found after H 2 administrated. Inhibition of mTOR may be involved in the upregulation of autophagy by H 2. Finally, increased phosphorylation of p38 and JNK was involved in the CIH-induced pathological process. H 2 could inhibit the activation of p38 and JNK, suggesting H 2 played an active part in resisting renal injury via MAPK. Significance Taken together, our study reveals that H 2 can ameliorate CIH-induced kidney injury by decreasing endoplasmic reticulum stress and activating autophagy through inhibiting oxidative stress-dependent p38 and JNK MAPK activation. [ABSTRACT FROM AUTHOR]