Research ReportDiazoxide promotes oligodendrocyte differentiation in neonatal brain in normoxia and chronic sublethal hypoxia

- Diazoxide increases oligodendrocyte differentiation in the cerebral white matter.
- Diazoxide promotes the expression of transcriptional factors, Nkx2.2 and Sox10 in normoxia.
- Diazoxide increases the expression of myelin genes, CNP and MBP, in normoxia.

Periventricular white matter injury (PWMI) is the most common cause of brain injury in preterm infants. It is believed that loss of late oligodendrocyte progenitor cells (OPCs) and disrupted maturation of oligodendrocytes contributes to defective myelination in PWMI. At present, no clinically approved drugs are available for treating PWMI. Previously, we found that diazoxide promotes myelination and attenuates brain injury in the chronic sublethal hypoxia model of PWMI. In this study, we investigated the mechanisms by which diazoxide promotes myelination. We observed that diazoxide increases the ratio of differentiated oligodendrocytes in the cerebral white matter, promotes the expression of differentiation-associated transcriptional factors Nkx2.2 and Sox10, and increases the expression of myelin genes CNP and MBP. These results show that diazoxide promotes oligodendrocyte differentiation in the developing brain.