Preterm infant born under 32 weeks of gestational age are at a high risk of white matter brain injury (WMI). This thesis used a fetal sheep model of brain injury induced by hypoxia-ischemia (HI) at a developmental age equivalent to approximately 28-32 weeks brain development in the human infant. The data presented in this thesis demonstrates that whole white blood cell fraction of cells derived from term and preterm UCB, and ex-vivo expanded UCB-MSC, modified fetal brain damage after HI insult. Cells derived from UCB are an effective neuroprotective strategy, principally acting via a decrease in neuroinflammation to protect preterm brain development after HI. UCB-MSC also appears to be effective for neuroregeneration, acting via central anti-inflammatory and cerebral chemokine modulation. Combined, these results strongly suggest that UCB cells could be used to reduce WMI in the preterm brain.