Recombinant Human Erythropoietin Augments Neovascularization Responses in a Neonatal Rat Model of Premature Brain Damage by Phosphatidylinositol 3 Kinase/Akt Pathway.

-pdf-only no pmc-prop-suppress-copyright no pmc-prop-is-real-version no pmc-prop-is-scanned-article no pmc-prop-preprint no pmc-prop-in-epmc yes pmc-license-ref CC BY-NC-SA I ntroduction Incidence and mortality of neonatal-acquired brain damage, especially hypoxic-ischemic brain damage (HIBD), have an increasing trend.[ 1 ] Brain damage of prematurity is the predominant form of the acquired brain damage in neonates who undergo neurological morbidity.[ 2 ] There are only limited therapies to improve the outcome from the HIBD.[ 3 ] Administration of the recombinant human-erythropoietin (rh-EPO) into extremely preterm infants at Neonatal Intensive Care Unit improved neurodevelopmental outcomes.[ 4 ] However, the underlying mechanisms that support the neuroprotective effects of the rh-EPO following premature brain damage remain unclear.

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