G-CSF attenuates neuroinflammation and stabilizes the blood-brain barrier via the PI3K/Akt/GSK-3 beta signaling pathway following neonatal hypoxia-ischemia in rats

摘要

Objective: Neonatal hypoxia occurs in approximately 60% of premature births and is associated with a multitude of neurological disorders. While various treatments have been developed, translating them from bench to bedside has been limited. We previously showed G-CSF administration was neuroprotective in a neonatal hypoxia-ischemia rat pup model, leading us to hypothesize that G-CSF inactivation of GSK-3 beta via the PI3K/Akt pathway may attenuate neuroinflammation and stabilize the blood-brain barrier (BBB).