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Granulocyte‐Colony Stimulating Factor Exerts Neuroprotection in the Neonatal Hypoxia‐Ischemia Rat Model via the Hypothalamic‐Pituitary‐Adrenal Axis

Neonatal hypoxia ischemia (HI) remains the leading cause of perinatal brain injury affecting 60% of preterm infants. Several reports suggest that the activity of the hypothalamic‐pituitary‐adrenal (HPA) axis is increased after HI. Granulocyte‐colony‐stimulating factor (G‐CSF) is a neuroprotective drug shown to modulate the HPA axis in the adult rat by regulating the adrenocorticotropic hormone (ACTH) and corticosterone (CORT). We hypothesize that G‐CSF confers neuroprotection in neonatal HI by suppressing the activity of the HPA axis. To test the hypothesis Metyrapone (MET), a CORT synthesis inhibitor, and dexamethasone (DEX,) a synthetic glucocorticoid, was administered separately or in combination with G‐CSF. HI was induced in P7 rats following a modified Rice‐Vanucci model, which were randomly assigned to groups and treated one hour after HI. We report that G‐CSF is neuroprotective in neonatal HI by reducing infarct volume, and regulating CORT levels. The combination of G‐CSF and MET increased weight gain, and significantly decreased pro‐apoptotic markers in the brain; while DEX reversed the effects of G‐CSF.