Abstract

Neonatal hypoxic-ischaemic encephalopathy (HIE) is a neurological disease that can cause neonatal death. MicroRNA-124-3p (miR-124-3p) plays an important role in the development of various diseases. In this research, our aim was to investigate the potential function of miR-124-3p in regulating HIE and to find the underlying mechanism. Here, we discovered that miR-124-3p expression was reduced and cell apoptosis was increased in HIE rat model group. Interestingly, we identified that B cell lymphoma-2-associated X protein (Bax) was a direct target gene of miR-124-3p and Bax expression was negatively modulated by miR-124-3p in HIE. Functional experiments showed that miR-124-3p expression was reduced and Bax expression was increased in oxygen and glucose deprivation (OGD)-treated neurons. In addition, the cell viability of neurons was decreased and apoptosis was increased after OGD treatment. And miR-124-3p over-expression promoted cell viability and restrained apoptosis of the OGD-treated neurons. All these effects were reversed by Bax over-expression. Our results indicated that over-expression of miR-124-3p attenuated OGD-induced neuronal injury through targeting Bax, suggesting a potential role of miR-124-3p/Bax in the pathophysiology of HIE.

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