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目的:用β-淀粉样蛋白(Aβ_(25-35))诱导PC-12细胞凋亡以建立阿尔茨海默病细胞模型。方法:体外培养大鼠嗜铬细胞瘤PC-12细胞,以不同浓度Aβ_(25-35)诱导并于不同时间收获细胞,应用MTT法观察细胞活力,Fura-2/AM荧光分析法检测细胞内游离Ca~(2+)浓度,Hoech-st33258及碘化丙啶复染分析细胞凋亡。结果:Aβ_(25-35)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;同时细胞内Ca~(2+)浓度显著上升;不同浓度Aβ_(25-35)作用后,PC-12细胞于不同时间出现凋亡的典型形态学特征,该时间比Ca~(2+)浓度上升约晚6-12 h。结论:Aβ_(25-35)诱导PC-12细胞活力下降、细胞内Ca~(2+)浓度上升及细胞凋亡,可作为较理想的阿尔茨海默病细胞模型。
AIM: To induce apoptosis of PC-12 cells with β-amyloid (Aβ 25-35) to establish a cell model of Alzheimer’s disease. Methods: The rat pheochromocytoma PC-12 cells were cultured in vitro. Cells were harvested at different concentrations of Aβ 25-35 and harvested at different time. Cell viability was observed by MTT assay. Fura-2 / AM fluorescence assay was used to detect intracellular Free Ca ~ (2+) concentration, Hoech-st33258 and propidium iodide were used to analyze apoptosis. Results: After treated with Aβ 25-35, the cell viability decreased gradually and in a time and dose dependent manner. At the same time, the intracellular Ca 2+ concentration increased significantly. Aβ 25-35, After treatment, PC-12 cells showed typical morphological characteristics of apoptosis at different times, which was about 6-12 h later than Ca 2+ concentration. CONCLUSION: Aβ_ (25-35) can induce PC-12 cell viability decline, intracellular Ca 2+ concentration increase and apoptosis in PC12 cells, which may be an ideal cell model of Alzheimer’s disease.