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β-淀粉样多肽增加PC12细胞对钙的摄取:这可能是其在阿尔茨海默病中产生细胞毒性的一种机制。

beta-Amyloid polypeptide increases calcium-uptake in PC12 cells: a possible mechanism for its cellular toxicity in Alzheimer's disease.

作者信息

Fukuyama R, Wadhwani K C, Galdzicki Z, Rapoport S I, Ehrenstein G

机构信息

Laboratory of Neurosciences, National Institute on Aging, NIH, Bethesda, MD 20892.

出版信息

Brain Res. 1994 Dec 26;667(2):269-72. doi: 10.1016/0006-8993(94)91505-9.

Abstract

Calcium-uptake into PC12 cells was measured by incubation with 45Ca after the cells were exposed for 24 h to beta-amyloid peptide(1-40) at concentrations between 0 and 46 microM. The rate of influx of 45Ca into PC12 cells was constant for the first 10 min. For 46 microM beta-amyloid peptide(1-40), the rate of influx was about 1,300 ions/s/microns 2 and the number of cells decreased significantly. There was no significant decrease in cell number when cells were exposed to beta-amyloid in calcium-free medium. These results indicate that beta-amyloid increases calcium uptake into PC12 cells, and suggest that the increased uptake is responsible for the toxicity of beta-amyloid in PC12 cells.

摘要

在PC12细胞暴露于浓度为0至46微摩尔的β-淀粉样肽(1-40)24小时后,通过与45Ca孵育来测量PC12细胞对钙的摄取。在最初的10分钟内,45Ca进入PC12细胞的流入速率是恒定的。对于46微摩尔的β-淀粉样肽(1-40),流入速率约为1300个离子/秒/微米2,并且细胞数量显著减少。当细胞在无钙培养基中暴露于β-淀粉样肽时,细胞数量没有显著减少。这些结果表明,β-淀粉样肽增加了PC12细胞对钙的摄取,并表明摄取增加是β-淀粉样肽对PC12细胞毒性的原因。

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