Exogenous Brain-Derived Neurotrophic Factor at a 50 ng/mL Concentration has a Significant Protective Effect on Bilirubin-Induced Cerebral Cortex Neuronal Injury.

Abstract

Bilirubin encephalopathy is a common disabling disease in neonates. Brain-derived neurotrophic factor (BDNF) plays an important role in the repair and regeneration of nerves following injury, as well as the maintenance of neuronal growth and differentiation. This study aimed to investigate the effect of exogenous BDNF on the apoptosis and survival of in vitro cultured neurons injured by bilirubin as well as determine the optimal BDNF concentration. Rat cerebral cortex neurons cultured for 8 days were randomly divided into the control, bilirubin, and BDNF groups. A bilirubin injury model was established. BDNF was added to the BDNF group at a final concentration of 5, 50, and 100 ng/mL 4 hours prior to the addition of bilirubin. The cell morphology was observed via phase contrast microscopy, and the cell viability and apoptotic rate were detected using the methyl thiazolyl tetrazolium method and flow cytometry. The neuronal viability in the bilirubin group was significantly decreased and the apoptotic rate was significantly increased compared with the control group. BDNF significantly improved the impact of bilirubin on neuronal activity; the apoptotic rate was significantly decreased (p < 0.05); however, within 24 - 48 hours, BDNF had no significant effect on the nerve cell viability (p > 0.05). Moreover, the protective effect of different BDNF concentrations also varied (p < 0.05), with the most substantial protective effect at a final concentration of 50 ng/mL. Bilirubin may damage rat cerebral cortex neurons and induce their apoptosis, whereas BDNF has a protective effect on bilirubin-induced cerebral cortex neuronal injury.