论文部分内容阅读
目的:探讨β淀粉样蛋白1-42(Aβ1-42)促进转染人α-突触核蛋白(α-Syn)A53T突变基因的PC12细胞(A53T细胞)内α-Syn的表达及维生素C对A53T细胞保护作用的机制。方法:对高表达α-Syn的A53T细胞分别采用PBS、Aβ1-42和Aβ1-42+维生素C干预。用MTT法检测细胞活性和Western blot检测不同干预后A53T细胞α-Syn表达量。结果:①随着Aβ1-42浓度增加,细胞活性呈浓度依赖性降低;维生素C可减轻细胞损伤。②Western blot检测结果提示维生素C可减轻α-Syn的谱带密度;Aβ1-42干预后A53T细胞内α-Syn表达量相对值为(0.76±0.13),维生素C干预后α-Syn表达量相对值为(0.23±0.08),两者差异有统计学意义(P<0.01)。结论:Aβ1-42可导致高表达α-Syn的A53T细胞损伤,并促进α-Syn的表达;维生素C可部分拮抗该效应,对神经细胞具有一定的保护作用。
Objective: To investigate the effect of β-amyloid 1-42 (Aβ1-42) on the expression of α-Syn in PC12 cells (A53T cells) transfected with human α-Syn A53T gene and the effect of vitamin C on A53T cell protection mechanism. Methods: A53T cells highly expressing α-Syn were treated with PBS, Aβ1-42 and Aβ1-42 + vitamin C respectively. Cell viability was measured by MTT assay and Western blot was used to detect the expression of α-Syn in A53T cells. Results: ① With the increase of Aβ1-42 concentration, cell activity decreased in a concentration-dependent manner; Vitamin C reduced cell injury. ②Western blot results suggested that vitamin C could reduce the density of α-Syn; the relative expression of α-Syn in A53T cells after Aβ1-42 intervention was (0.76 ± 0.13), the relative expression of α-Syn after intervention with vitamin C (0.23 ± 0.08), the difference was statistically significant (P <0.01). CONCLUSION: Aβ1-42 can induce the injury of A53T cells with high expression of α-Syn and promote the expression of α-Syn. Vitamin C can partially antagonize this effect and have some protective effects on nerve cells.