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首页> 外文期刊>The European Journal of Neuroscience >Involvement of calcineurin in the neurotoxic effects induced by amyloid-beta and prion peptides.
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Involvement of calcineurin in the neurotoxic effects induced by amyloid-beta and prion peptides.

机译：钙调神经磷酸酶参与β-淀粉样蛋白和病毒肽诱导的神经毒性作用。

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摘要

It is usually accepted that prion and amyloid-beta (Abeta) peptides induce apoptotic cell death. However, the mechanisms that trigger neuronal death, induced by these amyloidogenic peptides, remain to be clarified. In the present study we analysed the neurotoxic effects of the synthetic prion and Abeta peptides, PrP106-126 and Abeta25-35, in primary cultures of rat brain cortical cells. PrP106-126 and Abeta25-35 incubated at a concentration of 25 micro m for 24 h, did not affect cell membrane integrity, but decreased the metabolic capacity of the cells. The intracellular free Ca2+ concentration and reactive oxygen species levels increased significantly after 24 h treatment with PrP106-126 and Abeta25-35. Furthermore, these peptides (after 24 h exposure) also induced cytochrome c release from mitochondria and increased caspase-3-like activity. FK506, an inhibitor of the Ca2+/calmodulin-dependent phosphatase, calcineurin, was able to prevent cytochrome c release, caspase-3 activation and cell death induced by Abeta25-35 or PrP106-126 peptides. Taken together these data suggest that calcineurin is involved in Abeta25-35 and PrP106-126 neurotoxicity.
机译：通常认为病毒和淀粉样蛋白（Abeta）肽会诱导凋亡性细胞死亡。然而，由这些淀粉样蛋白生成肽诱导的神经元死亡的机制仍有待阐明。在本研究中，我们分析了合成的ion病毒和Abeta肽PrP106-126和Abeta25-35在大鼠大脑皮层细胞的原代培养物中的神经毒性作用。 PrP106-126和Abeta25-35在25微米的浓度下孵育24小时，不会影响细胞膜的完整性，但会降低细​​胞的代谢能力。 PrP106-126和Abeta25-35处理24小时后，细胞内游离Ca2 +浓度和活性氧水平显着增加。此外，这些肽（暴露24 h后）还诱导线粒体释放细胞色素c，并增加caspase-3样活性。 FK506是Ca2 + /钙调蛋白依赖性磷酸酶钙调神经磷酸酶的抑制剂，能够预防Abeta25-35或PrP106-126肽诱导的细胞色素c释放，caspase-3活化和细胞死亡。这些数据加在一起表明钙调神经磷酸酶参与了Abeta25-35和PrP106-126的神经毒性。

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