β淀粉样蛋白致PC-12细胞损伤的研究  

Study on β-myloid's impairment action on PC-12

作　　者：聂靖炜[1] 李颖[1] 王瑞涛[1] 

机构地区：[1]哈尔滨医科大学第二临床医学院老年病科,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2007年第3期234-236,240,共4页Journal of Harbin Medical University

摘　　要：目的对β淀粉样蛋白致PC-12细胞的损伤进行初步研究。方法体外培养大鼠嗜铬细胞瘤PC-12细胞,以不同浓度β淀粉样蛋白(Aβ25-35)诱导PC-12细胞后,MTT法观察细胞活力,TUNEL法测细胞凋亡率,并用P-tau抗体检测异常磷酸化tau蛋白的表达。结果A2β5-35作用于PC-12细胞后,细胞活力逐渐下降,并呈时间和剂量依赖性,同时荧光显微镜观察到10μmol/L的A2β5-35作用于PC-12细胞24h,TUNEL阳性细胞实验组多于对照组,有统计学意义,P-tau阳性细胞实验组多于对照组,有统计学意义。结论Aβ25-35使PC-12细胞产生凋亡和tau蛋白异常磷酸化的形态学损伤。Objective A preliminary study on β-myloid＇s impairment action on PC-12.Methods The PC-12 cells were cultured in vitro and Aβ25-35 was added into the medium in different concentrations. Then MTT assay was used for observing the cell vitality, and cell apoptosis was detected by TdT-mediated biotinylated-dUTP nick end labeling（TUNEL） method. The expression of anormalously phosphorylated tau protein was tested with P-tan antibody. Results After being induced by Aβ25-35, the cell vitality was decreased in a time and dose-dependent manner. PC-12 cells could be attected by 10 μmol/L of Aβ25-35 during 24 hours observed with fluorescence microscope. At that moment, TUNEL positive cells were more significantly in Aβ25-35 treated groups than that in control, and P-tan positive cells were also more significantly in Aβ25-35 treated groups than that in control. Conclusion Aβ25-35 could cause PC-12 apoptosis and P-tau anormalously phosphorylated.

关 键 词：Β淀粉样蛋白 PC12细胞 阿尔茨海默病 凋亡 P-tau蛋白 细胞培养 

分 类 号：Q813[生物学—生物工程]