MEG8 is involved in ischemia stroke, however, its role in ischemia stroke remains unknown. The current research aimed to investigate the effects and mechanisms of MEG8 in ischemic stroke. Mouse brain microvascular endothelial cells (BMECs) were treated by oxygen–glucose deprivation (OGD). Then, the expressions of MEG8 and miR-130a-5p were detected by quantitative reverse transcription-polymerase chain reaction (q-PCR). Cell counting kit-8 (CCK-8), wound-healing, tube formation, Western blot, and q-PCR assays were performed to detect the effects of MEG8 and miR-130a-5p on cell viability, migration, and angiogenesis and VEGFA expression. Bioinformatics, dual-luciferase reporter assay, and RNA immunoprecipitation analysis were carried out to investigate the targeting relationship between MEG8 and miR-130a-5p, and between miR-130a-5p and VEGFA. Then, rat middle cerebral artery occlusion (MCAO) model and MEG8 overexpression MCAO model were established, and neurological deficit and infarct volume of the model rats were evaluated. Finally, Western blot and q-PCR were carried out to detect the expressions of MEG8, miR-130a-5p, and VEGFA. MEG8 was upregulated and miR-130a-5p was downregulated in OGD-treated BMECs. MiR-130a-5p was found to be a target of MEG8, and VEGFA was predicted to be a potential target of miR-130a-5p. Downregulation of MEG8 inhibited the cell viability, migration, and angiogenesis and the expression of VEGFA via negatively regulating miR-130a-5p of BMECs treated by OGD/non-OGD. In addition, MEG8 reduced cerebral ischemia, neurological score and miR-130a-5p expression, and increased VEGFA expression of MCAO rat. Our findings proved that MEG8 regulates angiogenesis and attenuates cerebral ischemia after ischemic stroke via miR-130a-5p/VEGFA signaling.

MEG8 参与缺血性中风，然而，其在缺血性中风中的作用尚不清楚。目前的研究旨在探讨 MEG8 在缺血性卒中中的作用和机制。小鼠脑微血管内皮细胞（BMECs）通过氧-葡萄糖剥夺（OGD）进行治疗。然后，通过定量逆转录-聚合酶链反应（q-PCR）检测 MEG8 和 miR-130a-5p 的表达。使用细胞计数试剂盒-8 (CCK-8)、伤口愈合、管形成、蛋白质印迹和 q-PCR 测定检测 MEG8 和 miR-130a-5p 对细胞活力、迁移、血管生成和 VEGFA 的影响表达。通过生物信息学、双荧光素酶报告基因检测和 RNA 免疫沉淀分析，研究 MEG8 与 miR-130a-5p 以及 miR-130a-5p 与 VEGFA 之间的靶向关系。然后，建立大鼠大脑中动脉闭塞（MCAO）模型和MEG8过表达MCAO模型，评估模型大鼠的神经功能缺损和梗死体积。最后，进行Western blot和q-PCR检测MEG8、miR-130a-5p和VEGFA的表达。在 OGD 处理的 BMEC 中，MEG8 被上调，而 miR-130a-5p 被下调。发现 MiR-130a-5p 是 MEG8 的靶标，并且预测 VEGFA 是 miR-130a-5p 的潜在靶标。MEG8的下调通过负调节OGD/非OGD处理的BMEC的miR-130a-5p来抑制细胞活力、迁移和血管生成以及VEGFA的表达。此外，MEG8降低了MCAO大鼠的脑缺血、神经系统评分和miR-130a-5p的表达，并增加了VEGFA的表达。