Protective effects of FGF10 on neurovascular unit in a rat model of neonatal hypoxic-ischemic brain injury.

Neonatal hypoxic-ischemic (HI) brain injury remains a devastating clinical disease associated with high mortality and lifetime disability. Neonatal HI injury damages the architecture of neurovascular unit (NVU), thus, therapy targeting the NVU may provide effective neuroprotection against HI. This study was designed to investigate whether fibroblast growth factor 10 (FGF10) protected the NVU against HI and afforded observable neuroprotection in a rat model of neonatal HI brain injury. The results showed that FGF10 treatment significantly reduced brain damage post HI, characterized by reduction in brain infarct volume and tissue loss. Further interesting findings showed that FGF10 treatment exerted neuroprotective effects on HI brain injury in neonate rats through protecting the NVU against HI, evidenced by inhibition of neuronal cell apoptosis, suppression of gliosis, and amelioration of blood-brain barrier disruption. Collectively, our study indicates that FGF10 treatment exhibits great potential for protecting NVU against HI and attenuates neonatal brain injury, suggesting a potential novel therapeutic agent to this disease. • FGF10 decreases neuronal death via inhibiting neuronal apoptosis • FGF10 attenuates the activation of microglia and astrocytes through modulating TLR4/NF-κB signaling pathway • FGF10 ameliorates blood-brain barrier disruption via reducing tight junction and adherens junction proteins degradation and pericytes loss • FGF10 exerts protective effects on the neurovascular unit in a rat model of neonatal HI brain injury. [ABSTRACT FROM AUTHOR]