铝增加神经母细胞瘤中β -淀粉样蛋白和泛素的水平,但在神经胶质瘤细胞中没有。

A Campbell, A Kumar, F G La Rosa, K N Prasad, S C Bondy
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引用次数: 48

摘要

一些流行病学研究表明,铝(Al)参与阿尔茨海默病(AD)的发病机制。阿尔茨海默病病理病变中β和泛素水平升高。因此,我们研究了铝(Al)处理是否会改变小鼠神经母细胞瘤(NBP2)和大鼠胶质瘤(C-6)细胞培养中β和泛素的水平。在低浓度(10微米)硫酸铝刺激NBP2细胞的免疫反应性β和泛素水平,但不改变淀粉样前体蛋白(APP)的水平。然而,在更高的浓度(100和500微米)下,铝没有对β -淀粉样蛋白产生任何显著影响,而泛素水平继续增加。用任何浓度的Al处理后,C-6胶质瘤细胞中的β和泛素含量均未发生变化。将细胞暴露于铝盐中并没有改变两种细胞系的增殖速度。这些数据表明,Al可能在AD中发挥作用的机制之一是通过促进神经元中β和泛素的形成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aluminum increases levels of beta-amyloid and ubiquitin in neuroblastoma but not in glioma cells.

Several epidemiological studies suggest the involvement of aluminum (Al) in the pathogenesis of Alzheimer's disease (AD). There is an increase in the levels of Abeta and ubiquitin in the pathological lesions of AD. Therefore, we have investigated whether aluminum (Al) treatment alters the levels of Abeta and ubiquitin in murine neuroblastoma (NBP2) and rat glioma (C-6) cell cultures. At a low concentration (10 microM), aluminum sulfate stimulated the level of immunoreactive Abeta and ubiquitin in NBP2 cells without changing the levels of the amyloid precursor protein (APP). However, at higher concentrations (100 and 500 microM), aluminum failed to elicit any significant effect on beta-amyloid, whereas ubiquitin levels continued to increase. No changes in the Abeta and ubiquitin content were found in the C-6 glioma cells following treatment with Al at any of the concentrations tested. Exposure of cells to aluminum salts did not alter the rate of proliferation in either of the two cell lines. These data suggest that one of the mechanisms by which Al may play a role in AD is by promoting the formation of Abeta and ubiquitin in neurons.

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