Cerebral ischemia/reperfusion (I/R) can lead to serious brain function impairments. Long noncoding RNA (lncRNA) CCAAT enhancer binding protein α antisense RNA 1 (CEBPA-AS1) was shown to be upregulated in human ischemic stroke. This work investigated the function and mechanism of CEBPA-AS1 in I/R. An oxygen-glucose deprivation/reperfusion (OGD/R) model was used to induce I/R injury in SH-SY5Y cells in vitro. RT-qPCR examined the expression of CEBPA-AS1, microRNA-24-3p (miR-24-3p), and Bcl-2-related ovarian killer (Bok). The cell viability, apoptosis, oxidative stress in OGD/R-treated cells were detected using CCK-8, flow cytometry, western blot, ELISA assays. The relationship among genes was tested by RNA pulldown and luciferase reporter assays. We found that OGD/R upregulated CEBPA-AS1 expression in SH-SY5Y cells. Functionally, CEBPA-AS1 depletion ameliorated OGD/R-induced apoptosis and oxidative stress in SH-SY5Y cells by reducing ROS production and superoxide dismutase (SOD) and glutathione (GSH). Mechanistic investigations indicated that CEBPA-AS1 acts as a sponge for miR-24-3p, and miR-24-3p binds to the BOK. Moreover, miR-24-3p upregulation or BOK downregulation antagonized the protective role of CEBPA-AS1 depletion in SH-SY5Y cells exposed to OGD/R. Overall, downregulation of CEBPA-AS1 exerts protective functions against OGD/R-induced injury by targeting the miR-24-3p/BOK axis.

中文翻译：

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CEBPA-AS1 敲低通过 miR-24-3p/BOK 轴减轻 OGD/R 诱导的神经元细胞损伤

脑缺血/再灌注 (I/R) 可导致严重的脑功能障碍。长链非编码 RNA (lncRNA) CCAAT 增强子结合蛋白 α 反义 RNA 1 ( CEBPA-AS1 ) 在人类缺血性中风中被上调。这项工作研究了CEBPA-AS1在 I/R 中的功能和机制。使用氧-葡萄糖剥夺/再灌注（OGD/R）模型在体外诱导SH-SY5Y细胞的I/R损伤。RT-qPCR 检测CEBPA-AS1的表达、microRNA-24-3p (miR-24-3p) 和 Bcl-2 相关的卵巢杀手 (Bok)。使用 CCK-8、流式细胞术、蛋白质印迹、ELISA 测定法检测 OGD/R 处理的细胞中的细胞活力、凋亡、氧化应激。基因之间的关系通过 RNA 下拉和荧光素酶报告基因分析进行了测试。我们发现 OGD/R 上调SH-SY5Y 细胞中CEBPA-AS1的表达。在功能上，CEBPA-AS1消耗通过减少 ROS 产生和超氧化物歧化酶 (SOD) 和谷胱甘肽 (GSH) 改善了 OGD/R 诱导的 SH-SY5Y 细胞凋亡和氧化应激。机理研究表明，CEBPA-AS1充当 miR-24-3p 的海绵，而 miR-24-3p 与 BOK 结合。此外，miR-24-3p 上调或 BOK 下调拮抗暴露于 OGD/R 的 SH-SY5Y 细胞中的CEBPA-AS1消耗。总体而言，CEBPA-AS1的下调通过靶向 miR-24-3p/BOK 轴对 OGD/R 诱导的损伤发挥保护作用。