Laboratory of Neurobiology and State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing, China.
J Alzheimers Dis. 2010;19(2):529-44. doi: 10.3233/JAD-2010-1246.
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 (Abeta)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 Abeta 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.
甘丙肽和甘丙肽受体在上与阿尔茨海默病（AD）相关的大脑区域中上调。然而，这种过表达的后果仍不清楚，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β（Abeta）1-42 毒性以及包括 staurosporine、依托泊苷、过氧化氢和血清耗竭在内的其他损伤的可能保护作用，在培养的人原代神经元中。结果表明，甘丙肽在亚纳摩尔生理浓度下可抵抗细胞内 Abeta 细胞毒性和所有上述损伤。甘丙肽的保护作用可能通过甘丙肽受体 2 和 Bax 水平的下调来介导。本研究的数据为治疗或预防包括 AD 在内的神经退行性疾病提供了一个潜在的药物靶点。
