Ischemic stroke is a common cerebrovascular disease caused by insufficient blood supply to the brain. In recent years, studies have demonstrated that microRNAs (miRNAs) are involved in a variety of biological processes in the nervous system. However, the effects of miR-202-5p on cerebral ischemic stroke injury have not been completely elucidated. In our study, N2a cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) treatment, and middle cerebral artery occlusion (MCAO) rat models were constructed. Our results indicated that decreased miR-202-5p expression was connected to N2a cells after OGD/R-induced injury and rats after MCAO. In addition, high miR-202-5p expression increased proliferation and prevented apoptosis and autophagy of OGD/R-treated N2a cells, while also effectively decreasing the infarct volume in MCAO model rats. We validated the interplay between miR-202-5p and eukaryotic translation initiation factor 4E (eIF4E), and found that miR-202-5p downregulated eIF4E by targeted combination. Moreover, we demonstrated that miR-202-5p accelerated proliferation and suppressed autophagy of OGD/R-induced N2a cells by targeting eIF4E. Meanwhile, our other results suggest that upregulation of miR-202-5p may activate the Akt/GSK-3β pathway in ischemic brain injury. Our findings suggest that miR-202-5p may serve as a protective agent for ischemia-reperfusion injury in stroke via eIF4E.

中文翻译：

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通过靶向eIF4E介导的自噬诱导和Akt /GSK-3β途径的抑制，MiR-202-5p减轻了MCAO模型大鼠的神经功能缺损和神经元损伤，以及OGD诱导的Neuro-2a细胞损伤。

缺血性中风是由脑供血不足引起的常见脑血管疾病。近年来，研究表明，microRNA（miRNA）参与神经系统的多种生物学过程。但是，尚未完全阐明miR-202-5p对脑缺血性中风损伤的作用。在我们的研究中，对N2a细胞进行了氧葡萄糖剥夺/复氧（OGD / R）处理，并构建了大脑中动脉闭塞（MCAO）大鼠模型。我们的结果表明，降低的miR-202-5p表达与OGD / R诱导的损伤和MCAO后的大鼠的N2a细胞有关。此外，高miR-202-5p表达可增加增殖，并防止OGD / R处理的N2a细胞凋亡和自噬，同时还可以有效降低MCAO模型大鼠的梗塞体积。我们验证了miR-202-5p与真核翻译起始因子4E（eIF4E）之间的相互作用，并发现miR-202-5p通过靶向组合下调了eIF4E。此外，我们证明了miR-202-5p通过靶向eIF4E来加速增殖并抑制OGD / R诱导的N2a细胞自噬。同时，我们的其他结果表明，miR-202-5p的上调可能激活缺血性脑损伤中的Akt /GSK-3β途径。我们的发现表明，miR-202-5p可能通过eIF4E充当中风缺血再灌注损伤的保护剂。我们证明了miR-202-5p通过靶向eIF4E来加速增殖并抑制OGD / R诱导的N2a细胞自噬。同时，我们的其他结果表明，miR-202-5p的上调可能激活缺血性脑损伤中的Akt /GSK-3β途径。我们的发现表明，miR-202-5p可能通过eIF4E充当中风缺血再灌注损伤的保护剂。我们证明了miR-202-5p通过靶向eIF4E来加速增殖并抑制OGD / R诱导的N2a细胞自噬。同时，我们的其他结果表明，miR-202-5p的上调可能激活缺血性脑损伤中的Akt /GSK-3β途径。我们的发现表明，miR-202-5p可能通过eIF4E充当中风缺血再灌注损伤的保护剂。