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Neonatal hypoxic-ischemic brain injury (HIBI) can lead to white matter damage, which significantly contributes to cognitive dysfunction, emotional disorders, and sensorimotor impairments. Although dexmedetomidine enhances neurobehavioral outcomes, its impact on oligodendrocyte genesis and myelination following hypoxic-ischemic events, as well as the underlying mechanisms, remain poorly understood. Dexmedetomidine was administered 15 min post-HIBI.

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