Intermittent hypoxic conditioning restores neurological dysfunction of mice induced by long-term hypoxia

BackgroundCentral nervous system diseases are associated with hypoxia, which usually cause irreversible nerve damage, but the underlying mechanism is unclear and effective intervention strategies are lacking. This study was designed to explore the mechanism and treatment strategy of hypoxia-induced nerve injury. MethodsIn this study, 13% O-2 was used to treat mice for 0, 1, 3 7, and 14 days, Morris water maze and other animal behavior experiments were used to evaluate the neurological function of mice. TUNEL, BrdU, PCNA, DCX, and SOX2 staining were used to observe the apoptosis and proliferation of mouse neurons. RT-PCR and Iba1 staining were used to evaluate the release of inflammatory factors IL-1 beta, IL-6, and TNF-alpha and the activation of microglia. ResultsShort-term hypoxia promotes neurogenesis, while long-term hypoxia inhibits neurogenesis. The changes in hypoxia-induced neurogenesis were positively correlated with neurological functions, but negatively correlated with apoptosis. Moreover, intermittent hypoxic conditioning restored long-term hypoxia-induced neurological dysfunction by promoting neural stem cell generation and inhibiting the release of inflammatory factors IL-1 beta, IL-6, and TNF-alpha and the activation of microglia. ConclusionHypoxia promoted neurogenesis in a time-dependent manner, and intermittent hypoxic conditioning exerted a neuroprotective effect through promoting neural stem cell generation and suppressing inflammation induced by long-term hypoxia stress, which provided a novel concept to develop a treatment for hypoxia-related brain injury.

Automated summary

This study investigated the mechanism and treatment strategy for hypoxia-induced nerve injury. The researchers found that short-term hypoxia promotes neurogenesis, while long-term hypoxia inhibits neurogenesis. Intermittent hypoxic conditioning showed a neuroprotective effect by promoting neural stem cell generation and suppressing inflammation induced by long-term hypoxia stress. This study provides a new concept for the treatment of hypoxia-related brain injury.