MALAT1介导β-catenin通路参与Salvinorin A减轻脑卒中后血脑屏障损伤的机制

【摘要】目的探讨MALAT1介导β-catenin通路参与Salvinorin A减轻脑卒中后血脑屏障（BBB）损伤的机制。方法选取SD大鼠制作大脑中动脉栓塞模型（MCAO），进行Salvinorin A减轻脑卒中后脑损伤相关实验。 选取人脑微血管内皮细胞（HBMECs）制作糖氧剥夺（OGD）模型，进行MALAT1介导β-catenin通路参与Salvinorin A脑保护机制的相关实验。结果Salvinorin A可明显减轻缺血再灌注后的神经功能损伤，脑水肿，BBB通透性破坏和内皮细胞损伤；而MALAT1干扰后Salvinorin A对内皮细胞的保护和β-catenin的促表达等作用被阻断。结论Salvinorin A可能通过调控内皮细胞中LncRNA-MALAT1表达，促进β-catenin的表达来减轻内皮细胞损伤，进而减轻缺血再灌注后的BBB损伤。

Abstract: Objective To investigate the mechanism of MALAT1-mediated β-catenin pathway involved in Salvinorin A moderates blood brain barrier（BBB） injury after stroke. MethodsSD rats were selected to make middle cerebral artery embolization model(MCAO) for the related detection experiment of Salvinorin A alleviating brain injury after stroke. Human microvascular endothelial cells(HBMECs) were selected to make glucose oxygen deprivation(OGD) model, and the relevant experiments on the role of MALAT1-mediated β-catenin pathway in the brain protective mechanism of Salvinorin A were conducted. ResultsSalvinorin A could significantly reduce the neurological damage, cerebral edema, damage of BBB permeability and endothelial cell injury after ischemia/reperfusion. However, after MALAT1 interference, the protective effect of Salvinorin A on endothelial cells and the promotion of β-catenin expression were blocked. ConclusionSalvinorin A may reduce the injury of endothelial cells by regulating the expression of lncRNA-MALAT1 in endothelial cells and promoting the expression of β-catenin, thus alleviating the injury of BBB after ischemia/reperfusion.