非肌肉肌球蛋白ⅡA维持高糖诱导的脑微血管内皮细胞功能OA

Objective:To investigate the mechanism of non-muscle myosin ⅡA(NMⅡA)in high glucose(HG)-induced in-jury of brain microvascular endothelial cells bEnd.3.Methods:An in vitro diabetic cerebrovascular injury model was established by culturing bEnd.3 cells in HG medium.NMⅡA expression was knocked down using siRNA,followed by assessments of cell viabil-ity,inflammatory factors,oxidative stress markers,and cellular morphological changes.Functional assays(CCK-8,wound heal-ing,atomic force microscopy)were performed to evaluate proliferation,migration,invasion,and mechanical properties.Protein and gene expression were analyzed by Western blot and RT-qPCR.Results:The HG-induced bEnd.3 model was successfully es-tablished.NMⅡA knockdown exacerbated inflammation and oxidative stress,reduced cell viability and migration,and decreased cell height,adhesion,and Young's modulus(P<0.05).Conclusion:NMⅡA regulates critical processes including cell contrac-tion,migration,and tension maintenance.Under HG conditions,NMⅡA deficiency worsens inflammation and impairs endotheli-al function,suggesting its pivotal role in preserving cerebrovascular homeostasis(P<0.05).Targeting NMⅡA may offer a novel therapeutic strategy for diabetic cerebrovascular complications.