基于PI3K/Akt/GSK3β信号通路的芥子酸抗Aβ1-42致PC12细胞损伤的机制研究
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篇名: 基于PI3K/Akt/GSK3β信号通路的芥子酸抗Aβ1-42致PC12细胞损伤的机制研究
TITLE: Study on the Mechanism of Sinapic Acid against PC 12 Cell Injury Induced by Aβ1-42 Based on PI 3K/Akt/GSK3β Signaling Pathway
摘要: 目的:基于磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(Akt)/糖原合成激酶3β(GSK3β)信号通路探讨芥子酸(SA)抗β淀粉样蛋白1-42(Aβ1-42)致PC12细胞损伤的作用机制。方法:将大鼠PC12细胞随机分为对照组、Aβ组(Aβ1-422μmol/L)、Aβ+SA组(Aβ1-422μmol/L+SA100μmol/L)、Aβ+SA+LY组[Aβ1-422μmol/L+SA100μmol/L+LY294002(PI3K抑制剂)10μmol/L]、Aβ+LY组(Aβ1-422μmol/L+LY29400210μmol/L)、LY组(LY29400210μmol/L)。除对照组、LY组外,其余各组细胞均以Aβ1-42复制损伤模型。培养24h后,使用显微镜观察各组细胞的形态,采用MTT法检测各组细胞的存活率;采用Westernblotting法检测各组细胞PI3K、p-PI3K、Akt、p-Akt、GSK3β、p-GSK3β蛋白的表达情况。结果:与对照组比较,Aβ组细胞数量变少、部分突触断裂消失,其存活率以及p-PI3K/PI3K、p-Akt/Akt、p-GSK3β/GSK3β比值均显著降低(P<0.05或P<0.01)。与Aβ组比较,Aβ+SA组细胞变圆、突触变多,其存活率以及p-PI3K/PI3K、p-Akt/Akt、p-GSK3β/GSK3β比值均显著升高(P<0.05)。与Aβ+SA组比较,Aβ+SA+LY组细胞部分突触断裂,其存活率以及p-PI3K/PI3K、p-Akt/Akt、p-GSK3β/GSK3β比值均显著降低(P<0.05);Aβ+LY组细胞碎片较多,其存活率虽有下降但差异无统计学意义,且p-PI3K/PI3K、p-Akt/Akt、p-GSK3β/GSK3β比值亦无明显变化(P>0.05)。单独给予LY294002对PC12细胞的形态、存活率以及p-PI3K/PI3K、p-Akt/Akt、p-GSK3β/GSK3β比值均无显著影响(P>0.05)。结论:SA可能通过激活PI3K/Akt/GSK-3β信号通路对Aβ1-42诱导的PC12细胞损伤发挥保护作用。
ABSTRACT: OBJECTIVE:To investigate the mechanism of sinapic acid (SA)against PC 12 cell injury induced by Amyloid β1-42 protein(Aβ1-42)based on PI 3K/Akt/GSK3β signaling pathway. METHODS:PC12 cells of rats were randomly divided into control group,Aβ group(Aβ1-42 2 μmol/L),Aβ+SA group(Aβ1-42 2 μmol/L+SA100 μmol/L),Aβ+SA+LY group [Aβ1-42 2 μmol/L+SA 100 μmol/L+LY294002(PI3K inhibitor )10 μmol/L],Aβ+LY group(Aβ1-42 2 μmol/L+LY294002 10 μmol/L)and LY group (LY294002 10 μmol/L). Except for control group and LY group ,the cells of other groups were replicated the damage model with Aβ1-42. After 24 hours of culture ,the morphology of cells was obsened in each group with a microscope ,and MTT assay was adopted to determine the cell viability of PC 12 cells in each group. Western blotting assay was used to detect the expression of PI 3K,p-PI3K, Akt,p-Akt,GSK3β and p-GSK3β in cells of each group. RESULTS:Compared with control group ,the number of cells decreased and some synaptic breaks disappeared in Aβ group while cell viability,ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK 3β/GSK3β in Aβ group were decreased significantly(P<0.05 or P<0.01). Compared with Aβ group,the cells became round and synapses became more in Aβ+SA group while cell viability,the ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK 3β/GSK3β were increased significantly(P<0.05). Compared with Aβ+SA group,some synaptic breaks occurred in Aβ+SA+LY group while cell viability, the ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK 3β/GSK3β were decreased significantly(P<0.05);Aβ+LY group had more cell debris,and t he cell viability was decreased ,but the difference was not significant ,and the ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK3 β/GSK3 β had no significant change (P>0.05); LY294002 alone had no significant effect on morphology ,cellviability and the ratio of p-PI 3K/PI3K,p-Akt/Akt or p-GSK 3β/ GSK3 β (P>0.05). CONCLUSIONS : SA may play aprotective role against PC 12 cell injury induced by A β 1-42 through activating PI 3K/Akt/GSK-3β.
期刊: 2020年第31卷第20期
作者: 薛迪,刘宇超,贾永明,汪娜,刘学伟
AUTHORS: XUE Di,LIU Yuchao,JIA Yongming,WANG Na,LIU Xuewei
关键字: 芥子酸;β淀粉样蛋白;磷脂酰肌醇-3-激酶/蛋白激酶B/糖原合成激酶3β信号通路;PC12细胞
KEYWORDS: Sinapic acid ;β-amyloid protein;PI3K/Akt/
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