Galanin Protects Against Intracellular Amyloid Toxicity in Human Primary Neurons
Galanin Protects Against Intracellular Amyloid Toxicity in Human Primary Neurons
复制标题
DOI：
10.3233/jad-2010-1246
复制
发表时间：
2010-01-01
影响因子：
4
通讯作者：
Zhang, Yan
中科院分区：
文献类型：
--
作者：
Cui, Jia;Chen, Qiuyue;Zhang, Yan
甘丙肽和甘丙肽受体在与阿尔茨海默病 (AD) 相关的大脑区域中表达上调。然而，这种过度表达的后果仍然未知，特别是在人类神经元中。在这里，我们研究了甘丙肽对细胞内淀粉样蛋白-β (A beta)(1-42) 毒性以及其他损伤（包括星孢菌素、依托泊苷、过氧化氢和培养的人原代神经元血清耗竭）的可能保护作用。结果表明，甘丙肽在亚纳摩尔生理浓度下可防止细胞内 Aβ 细胞毒性和所有上述损伤。甘丙肽保护作用可能是由甘丙肽受体2和Bax水平下调介导的。本研究的数据为治疗或预防神经退行性疾病（包括 AD）提供了潜在的药物靶点。
Galanin and galanin receptors are upregulated in the brain regions associated with Alzheimer's disease (AD). However, the consequence of this overexpression is still unknown, particularly in human neurons. Here, we investigate the possible protective effects of galanin against intracellular amyloid-beta (A beta)(1-42) toxicity, as well as other insults including staurosporine, etoposide, hydrogen peroxide, and serum depletion in cultured human primary neurons. The results show that galanin is protective against intracellular A beta cytotoxicity and all of the above insults at sub-nanomolar physiological concentrations. The galanin protection may be mediated by galanin receptor 2 and down-regulation of Bax level. The data from the present study provide a potential drug target for therapy or prevention of neurodegenerative diseases, including AD.