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目的:信号通路糖原合成酶激酶-3β(GSK-3β)在β淀粉样蛋白(Aβ)损伤脑微血管内皮细胞分泌Tau蛋白中的作用及通心络干预作用研究。方法:采用人脑微血管内皮细胞,随机分为正常组、模型组、通心络3个剂量组,通心络组细胞经通心络预处理6h后,除正常组,各组加入终浓度为20μmol·L-1的Aβ1-42干预24h诱导细胞损伤,检测经处理后内皮细胞上清液中Tau蛋白表达及内皮细胞中Tau蛋白及其信号通路GSK-3β的表达情况。结果:模型组内皮细胞中Tau蛋白及其信号通路GSK-3β的表达均增强,通心络组Tau蛋白表达及其信号通路GSK-3β的表达均减弱。结论:Aβ1-42可通过信号通路GSK-3β增强Tau蛋白的表达,而通心络降低Aβ1-42损伤的人脑微血管内皮细胞Tau蛋白表达可能通过抑制信号通路GSK-3β表达而实现的。
OBJECTIVE: The role of signal pathway glycogen synthase kinase-3β (GSK-3β) in the secretion of Tau protein by β-amyloid (Aβ) -induced cerebral microvascular endothelial cells and the intervention of Tongxinluo. Methods: The human brain microvascular endothelial cells were randomly divided into three groups: normal group, model group and Tongxinluo group. The cells in Tongxinluo group were pretreated with Tongxinluo for 6 hours, except for the normal group. The final concentration of each group was Aβ1-42 (20μmol·L-1) was used to induce cell injury 24h, and the expression of Tau protein in endothelial cells and the expression of GSK-3β in endothelial cells were detected. Results: The expression of Tau protein and its signal pathway GSK-3β in endothelial cells of model group were all increased, and the expression of Tau protein and GSK-3β in Tongxinluo group were weakened. CONCLUSION: Aβ1-42 enhances the expression of Tau protein through the signal pathway GSK-3β, and Tongxinluo reduces the expression of Tau protein in human cerebral microvascular endothelial cells induced by Aβ1-42 through inhibiting the expression of GSK-3β.