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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Preconditioning-induced protection against cyanide-induced neurotoxicity is mediated by preserving mitochondrial function.
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Preconditioning-induced protection against cyanide-induced neurotoxicity is mediated by preserving mitochondrial function.

机译：预处理诱导的针对氰化物诱导的神经毒性的保护作用是通过保持线粒体功能来介导的。

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摘要

The central nervous system is one of the main target organs in cyanide toxicity. In this study, primary cultures of chick embryonic neurons were used to characterize sodium cyanide (NaCN)-induced cell death and to investigate the mechanism of NaCN-mediated preconditioning. After treatment of the cells with 1mM NaCN for 1h followed by a NaCN-free incubation period of 23 h, we observed features of apoptosis such as a reduction in nuclear size, chromatin condensation and nuclear fragmentation as evaluated by nuclear staining with Hoechst 33258 and electron microscopy. In addition, NaCN-induced neurotoxicity was reduced by the protein synthesis inhibitor cycloheximide (CHX) suggesting an active type of cell death. Most of the neurons with condensed chromatin and a shrunken nuclei also showed membrane damage at a late stage. Mitochondrial membrane potential as well as the protein levels of Bcl-2 and Bcl-x(L) decreased 15-60 min and 1-3 h after the exposure to NaCN (1mM, 1h), respectively. Preconditioning caused by incubating chick neurons with 100 microM NaCN for 30 min followed by a NaCN-free interval of 24h significantly protected the neurons against subsequent NaCN (1mM, 1h)-induced damage. Preconditioning prevented NaCN-induced decrease in the mitochondrial membrane potential as well as in the protein levels of Bcl-2 and Bcl-x(L) suggesting that preconditioning-induced neuroprotection is mediated by preserving mitochondrial function.
机译：中枢神经系统是氰化物毒性的主要靶器官之一。在这项研究中，鸡胚神经元的原代培养被用来表征氰化钠（NaCN）诱导的细胞死亡，并研究NaCN介导的预处理机制。用1mM NaCN处理细胞1h，然后进行23h的无NaCN潜伏期后，我们观察到凋亡的特征，如核大小减小，染色质浓缩和核碎裂，如用Hoechst 33258和电子核染色所评估显微镜检查。此外，蛋白质合成抑制剂环己酰亚胺（CHX）降低了NaCN诱导的神经毒性，表明细胞死亡的活跃类型。大多数具有浓缩染色质和收缩核的神经元在后期也显示膜损伤。暴露于NaCN（1mM，1h）后15-60分钟和1-3小时，线粒体膜电位以及Bcl-2和Bcl-x（L）的蛋白质水平分别下降。将鸡神经元与100 microM NaCN孵育30分钟，然后无NaCN间隔24h进行预处理，可以显着保护神经元免受随后的NaCN（1mM，1h）诱导的损伤。预处理可预防NaCN诱导的线粒体膜电位以及Bcl-2和Bcl-x（L）蛋白质水平的降低，表明预处理诱导的神经保护作用是通过保持线粒体功能介导的。

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