In the current study, we reported that overexpression of miR-152-3p effectively ameliorated neurological deficits and protected blood-brain barrier(BBB) integrity in middle cerebral artery occlusion (MCAO) rats. In an in vitro model, the level of miR-152-3p was significantly decreased in bEnd.3 cells after oxygen–glucose deprivation/reperfusion (OGD/R) insult. miR-152-3p overexpressing bEnd.3 cell monolayers were protected from OGD/R-induced microvascular hyperpermeability. The miR-152-3p-mediated protective effect was associated with lower apoptosis of endothelia by negatively modulating the MAP3K2/JNK/c-Jun pathway.

在当前的研究中，我们报道了 miR-152-3p 的过表达有效地改善了大脑中动脉闭塞 (MCAO) 大鼠的神经功能缺陷并保护了血脑屏障 (BBB) 的完整性。在体外模型中，氧-葡萄糖剥夺/再灌注 (OGD/R) 损伤后 bEnd.3 细胞中 miR-152-3p 的水平显着降低。过表达 bEnd.3 的 miR-152-3p 单层细胞免受 OGD/R 诱导的微血管通透性过高的影响。miR-152-3p 介导的保护作用通过负向调节 MAP3K2/JNK/c-Jun 通路与内皮细胞凋亡减少相关。