Ischemic stroke is a nervous system disease with high rates of disability and mortality. MicroRNAs have been reported to modulate cerebral ischemia. The current study aimed to study the role of miR-361-3p in cerebral ischemia–reperfusion (I/R) injury. Experimental results revealed that miR-361-3p level was downregulated in a middle cerebral artery occlusion-induced ischemic stroke mouse model and in oxygen–glucose deprivation/reoxygenation-stimulated SH-SY5Y cells. After overexpressing miR-361-3p, the percentage of brain infarct volume and neurobehavioral scores in mice were significantly reduced, and the neuronal apoptosis was inhibited. Moreover, miR-361-3p overexpression could limit the production of reactive oxygen species (ROS). Furthermore, we investigated the underlying molecular mechanisms of miR-361-3p and identified that miR-361-3p combined with NACC1 3ʹUTR to negatively modulate its expression. In addition, NACC1 interacts with the PINK1/Parkin pathway in neurons. NACC1 overexpression could rescue the impacts of miR-361-3p mimics on cell apoptosis, ROS production and the PINK1/Parkin pathway. In conclusion, miR-361-3p could improve ischemia brain injury by targeting NACC1 through the PINK1/Parkin pathway. Therefore, miR-361-3p may serve as a potential therapeutic target for the brain injury after I/R.

缺血性中风是一种具有高致残率和死亡率的神经系统疾病。据报道，微小 RNA 可调节脑缺血。目前的研究旨在研究 miR-361-3p 在脑缺血再灌注 (I/R) 损伤中的作用。实验结果表明，在大脑中动脉闭塞诱导的缺血性卒中小鼠模型和氧-葡萄糖剥夺/复氧刺激的 SH-SY5Y 细胞中，miR-361-3p 水平下调。过表达miR-361-3p后，小鼠脑梗死体积百分比和神经行为评分显着降低，神经元凋亡受到抑制。此外，miR-361-3p 过表达可能会限制活性氧 (ROS) 的产生。此外，我们研究了 miR-361-3p 的潜在分子机制，并确定 miR-361-3p 与 NACC1 3ʹUTR 结合负调节其表达。此外，NACC1 与神经元中的 PINK1/Parkin 通路相互作用。NACC1 过表达可以挽救 miR-361-3p 模拟物对细胞凋亡、ROS 产生和 PINK1/Parkin 通路的影响。总之，miR-361-3p 可以通过 PINK1/Parkin 通路靶向 NACC1 来改善缺血性脑损伤。因此，miR-361-3p 可作为 I/R 后脑损伤的潜在治疗靶点。miR-361-3p 可通过 PINK1/Parkin 通路靶向 NACC1 来改善缺血性脑损伤。因此，miR-361-3p 可作为 I/R 后脑损伤的潜在治疗靶点。miR-361-3p 可通过 PINK1/Parkin 通路靶向 NACC1 来改善缺血性脑损伤。因此，miR-361-3p 可作为 I/R 后脑损伤的潜在治疗靶点。