In the present study, we aimed to illustrate the roles and working mechanisms of long non-coding RNA (lncRNA) rhabdomyosarcoma 2-associated transcript (Rmst) and EGb761 in oxygen–glucose deprivation (OGD)-induced brain microvascular endothelial cells (BMECs). OGD exposure augmented the level of Rmst while reduced the expression of miR-150 in bEnd.3 cells. MiR-150 could directly bind to Rmst in bEnd.3 cells. Rmst silencing abrogated the inhibitory influences on the proliferation and migration and the promoting impact on the apoptosis of bEnd.3 cells caused by OGD exposure. Rmst overexpression intensified OGD-induced injury in bEnd.3 cells. OGD induced the injury of bEnd.3 cells through Rmst/miR-150 axis. EGb761 attenuated the damage in bEnd.3 cells induced by OGD through targeting Rmst/miR-150 axis. EGb761 might be an effective therapeutic agent to protect brain microvascular endothelial cells from hypoxia–ischemia induced injury.

在本研究中，我们旨在阐明长非编码RNA（lncRNA）横纹肌肉瘤2相关转录本（Rmst）和EGb761在缺氧-葡萄糖剥夺（OGD）诱导的脑微血管内皮细胞（BMEC）中的作用和工作机制。OGD暴露可增加Rmst的水平，同时降低bEnd.3细胞中miR-150的表达。MiR-150可以直接与bEnd.3细胞中的Rmst结合。Rmst沉默消除了OGD暴露对bEnd.3细胞增殖和迁移的抑制作用以及对bEnd.3细胞凋亡的促进作用。Rmst过表达增强了bEnd.3细胞中OGD诱导的损伤。OGD通过Rmst / miR-150轴诱导bEnd.3细胞损伤。EGb761通过靶向Rmst / miR-150轴减轻了OGD对bEnd.3细胞的损伤。