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首页> 外文期刊>Life sciences >Blockage of amyloid beta peptide-induced cytosolic free calcium by fullerenol-1, carboxylate C60 in PC12 cells.
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Blockage of amyloid beta peptide-induced cytosolic free calcium by fullerenol-1, carboxylate C60 in PC12 cells.

机译：富勒烯醇-1（羧酸C60在PC12细胞中）对淀粉样β肽诱导的胞质游离钙的阻断。

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摘要

Amyloid beta protein (Abeta) alters signal transduction systems, including increases in the cytosolic free calcium ([Ca2+]i) response which have pathophysiological significance in Alzheimer's disease (AD). The purposes of this study were to elucidate the mechanism involved in Abeta's effect on the Ca2+ signal and to evaluate the effect of fullerenol-1, a water-soluble hydroxyl and superoxide radical scavenger, on the Abeta-induced Ca2+ response. Both Abeta and bradykinin (BK) dose-dependently elevated [Ca2+]i in PC12 cells. Fullerenol-1, at a concentration range between 100 nM and 1 microM, dose-dependently reduced the Abeta-induced [Ca2+]i response, but did not alter the subsequent BK-mediated process. Thapsigargin, an inhibitor of Ca2+-ATPase, released Ca2+ from the internal store and diminished the BK-mediated calcium spike but did not affect the Abeta-induced Ca2+ response. In the absence of extracellular calcium, the Abeta-induced, but not BK-induced, calcium spike was completely abolished. The Ca induced by Abeta did not enter through the voltage-dependent calcium channels or ligand gated calcium channels, because the peak of Abeta-evoked Ca2+ was not significantly altered by various Ca2+ channel blockers or a NMDA receptor antagonist MK801. In addition, neither cholera toxin nor pertussis toxin altered the Abeta-induced Ca response. The results demonstrated that Abeta-stimulated [Ca2+]i increase is due to Ca influx from an extracellular source rather than from the intracellular store. Alteration of the membrane lipid structure and permeability by free radicals generated by Abeta may be a major cause of Ca -influx. Furthermore, fullerenol-1, a novel antioxidant, may provide therapeutic benefits in neurodegenerative diseases such as AD.
机译：淀粉样蛋白β蛋白（Abeta）改变信号转导系统，包括增加胞质游离钙（[Ca2 +] i）反应，这在阿尔茨海默病（AD）中具有病理生理意义。这项研究的目的是阐明Abeta对Ca2 +信号的作用所涉及的机制，并评估Fullerenol-1（一种水溶性羟基和超氧化物自由基清除剂）对Abeta诱导的Ca2 +反应的影响。 Abeta和缓激肽（BK）在PC12细胞中均剂量依赖性地升高[Ca2 +] i。浓度范围在100 nM和1 microM之间的Fullerenol-1剂量依赖性地降低了Abeta诱导的[Ca2 +] i反应，但并未改变随后的BK介导的过程。 Thapsigargin是Ca2 + -ATPase的抑制剂，可从内部存储中释放Ca2 +，并减少BK介导的钙峰值，但不影响Abeta诱导的Ca2 +反应。在不存在细胞外钙的情况下，完全消除了Abeta诱导而不是BK诱导的钙峰值。 Abeta诱导的Ca不会通过电压依赖性钙通道或配体门控的钙通道进入，因为Abeta诱发的Ca2 +的峰并未被各种Ca2 +通道阻滞剂或NMDA受体拮抗剂MK801显着改变。此外，霍乱毒素和百日咳毒素均不能改变Abeta诱导的Ca反应。结果表明，Abeta刺激的[Ca2 +] i的增加是由于Ca从细胞外源而不是从细胞内储库流入。由Abeta产生的自由基引起的膜脂质结构和通透性的改变可能是Ca流入的主要原因。此外，新型抗氧化剂富勒烯醇1可以在神经退行性疾病（例如AD）中提供治疗益处。

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