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作 者:喻哲明[1] 丁正同[1] 任惠民[1] 邬剑军[1] 王坚[1] 陈嬿[1]
出 处:《中国临床神经科学》2011年第6期561-565,共5页Chinese Journal of Clinical Neurosciences
基 金:国家自然科学基金资助项目(编号:30872723)
摘 要: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。Aim: To observe the expression of α-synuclein in the PC12 cells transfected with human α-synuclein A53T mutation gene by the induction of amyloid-β1-42(Aβ1-42),as well as the protective effect of vitamin C.Methods: After the A53T cells were exposed to PBS,Aβ1-42 and Aβ1-42+vitamin C,the cell viabilities were detected through MTT and the expressions of α-synuclein were measured by the Western blot.Results: MTT assays showed that cell viabilities decreased concentration-dependently with the increase of Aβ1-42 concentration,while the vitamin C could alleviate the cell damage.Western blot examination suggested that Aβ1-42 promoted the expression of α-synuclein in A53T cells.The density of α-synuclein in Aβ1-42+ vitamin C treated cells was lower than that in Aβ1-42 treated cells.The relative values of α-synuclein level were 0.23 ± 0.08,0.76 ± 0.13,respectively.There was a significant difference in the α-synuclein levels between the two groups(P0.01).Conclusion: Through the anti-oxidative process,vitamin C could alleviate the A53T cell damage induced by Aβ1-42 and reduce the expression of α-synuclein,which may contribute to playing a role in protecting
关 键 词:PC12细胞 β淀粉样蛋白1-42 Α-突触核蛋白 维生素C
分 类 号:R742.5[医药卫生—神经病学与精神病学] Q189[医药卫生—临床医学]
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