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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/ |
| 阅读数： | 384 次 |
| 本月下载数： | 5 次 |
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