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首页> 外文期刊>The European Journal of Neuroscience >Involvement of oxidative stress and impaired lysosomal degradation in amiodarone-induced schwannopathy
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Involvement of oxidative stress and impaired lysosomal degradation in amiodarone-induced schwannopathy

机译：胺碘酮引起的神经痛的氧化应激和溶酶体降解受损

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摘要

Amiodarone hydrochloride (AMD), an anti-arrhythmic agent, has been shown to cause peripheral neuropathy; however, its pathogenesis remains unknown. We examined the toxic effects of AMD on an immortalized adult rat Schwann cell line, IFRS1, and cocultures of IFRS1 cells and adult rat dorsal root ganglion neurons or nerve growth factor-primed PC12 cells. Treatment with AMD (1, 5, and 10m) induced time- and dose-dependent cell death, accumulation of phospholipids and neutral lipids, upregulation of the expression of gangliosides, and oxidative stress (increased nuclear factor E2-related factor in nuclear extracts and reduced GSH/GSSG ratios) in IFRS1 cells. It also induced the upregulation of LC3-II and p62 expression, with phosphorylation of p62, suggesting that deficient autolysosomal degradation is involved in AMD-induced IFRS1 cell death. Furthermore, treatment of the cocultures with AMD induced detachment of IFRS1 cells from neurite networks in a time- and dose-dependent manner. These findings suggest that AMD-induced lysosomal storage accompanied by enhanced oxidative stress and impaired lysosomal degradation in Schwann cells might be a cause of demyelination in the peripheral nervous system.
机译：抗心律失常药盐酸胺碘酮（AMD）已被证明可引起周围神经病变。然而，其发病机理仍然未知。我们检查了AMD对永生化成年大鼠Schwann细胞系，IFRS1以及IFRS1细胞和成年大鼠背根神经节神经元或神经生长因子启动的PC12细胞的共培养物的毒性作用。用AMD（1、5和10m）处理可导致时间和剂量依赖性细胞死亡，磷脂和中性脂质蓄积，神经节苷脂表达上调以及氧化应激（核提取物和细胞中核因子E2相关因子增加）。降低IFRS1细胞中的GSH / GSSG比率）。它还诱导了LC3-II和p62表达的上调，并使p62磷酸化，这表明自溶酶体降解不足与AMD诱导的IFRS1细胞死亡有关。此外，用AMD处理共培养物会以时间和剂量依赖性方式诱导IFRS1细胞从神经突网络中脱离。这些发现表明，AMD诱导的溶酶体贮备，伴随着氧化应激增强和雪旺细胞中溶酶体降解受损，可能是周围神经系统脱髓鞘的原因。

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