褪黑激素介导的钙神经蛋白失活可减轻淀粉样β诱导的细胞凋亡

IF 2 Q3 NEUROSCIENCES
Jeong-Min Hong , Ali Newaz Munna , Ji-Hong Moon , Jae-Won Seol , Sang-Youel Park
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引用次数: 0

摘要

阿尔茨海默病(AD)是最常见的与年龄相关的进行性神经退行性疾病。淀粉样 beta 肽的积累是阿尔茨海默病的神经病理学标志。虽然褪黑素被认为对衰老和神经退行性疾病有保护作用,但褪黑素对钙调素酶在 AD 中的治疗作用却鲜为人知。在这项研究中,我们研究了褪黑素治疗对神经母细胞瘤细胞中淀粉样 beta 介导的神经毒性的影响及其潜在的分子机制。褪黑素治疗可减少神经母细胞瘤细胞中的钙调磷酸酶和自噬作用。电子显微镜图像显示,褪黑素抑制了淀粉样 beta 诱导的自噬空泡。与PrPC沉默的Zpl细胞相比,在表达PrPC的ZW细胞中更能观察到淀粉样β诱导的细胞凋亡率的增加。综上所述,这些结果表明,通过减轻钙神经蛋白和自噬通量激活的影响,褪黑素还能挽救淀粉样β诱导的神经毒性效应。这些发现可能与神经退行性疾病(包括注意力缺失症)的治疗有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Melatonin-mediated calcineurin inactivation attenuates amyloid beta-induced apoptosis

Alzheimer’s disease (AD) is the most common age-related progressive neurodegenerative disorder. The accumulation of amyloid beta-peptide is a neuropathological marker of AD. While melatonin is recognized to have protective effects on aging and neurodegenerative disorders, the therapeutic effect of melatonin on calcineurin in AD is poorly understood. In this study, we examined the effect and underlying molecular mechanisms of melatonin treatment on amyloid beta-mediated neurotoxicity in neuroblastoma cells. Melatonin treatment decreased calcineurin and autophagy in neuroblastoma cells. Electron microscopy images showed that melatonin inhibited amyloid beta-induced autophagic vacuoles. The increase in the amyloid beta-induced apoptosis rate was observed more in PrPC-expressing ZW cells than in PrPC-silencing Zpl cells. Taken together, the results suggest that by mitigating the effect of calcineurin and autophagy flux activation, melatonin could also rescue amyloid beta-induced neurotoxic effects. These findings may be relevant to therapy for neurodegenerative diseases, including AD.

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来源期刊
IBRO Neuroscience Reports
IBRO Neuroscience Reports Neuroscience-Neuroscience (all)
CiteScore
2.80
自引率
0.00%
发文量
99
审稿时长
14 weeks
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