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.

中文翻译：

---

microRNA-124-3p/Bax轴在新生儿缺氧缺血性脑病中的作用

摘要 新生儿缺氧缺血性脑病（HIE）是一种可导致新生儿死亡的神经系统疾病。MicroRNA-124-3p（miR-124-3p）在各种疾病的发生发展中起着重要作用。在这项研究中，我们的目的是研究 miR-124-3p 在调节 HIE 中的潜在功能并找到潜在的机制。在这里，我们发现HIE大鼠模型组miR-124-3p表达降低，细胞凋亡增加。有趣的是，我们发现 B 细胞淋巴瘤-2 相关 X 蛋白（Bax）是 miR-124-3p 的直接靶基因，并且 Bax 表达在 HIE 中受到 miR-124-3p 的负调节。功能实验表明，在氧和葡萄糖剥夺 (OGD) 处理的神经元中，miR-124-3p 表达降低，Bax 表达增加。此外，OGD处理后神经元细胞活力降低，细胞凋亡增加。并且 miR-124-3p 过表达促进了 OGD 处理的神经元的细胞活力并抑制了细胞凋亡。所有这些效果都被 Bax 过表达逆转了。我们的结果表明 miR-124-3p 的过表达通过靶向 Bax 减轻了 OGD 诱导的神经元损伤，表明 miR-124-3p/Bax 在 HIE 的病理生理学中具有潜在作用。