Advanced glycation endproducts induce changes in glucose consumption, lactate production, and ATP levels in SH-SY5Y neuroblastoma cells by a redox-sensitive mechanism
Advanced glycation endproducts induce changes in glucose consumption, lactate production, and ATP levels in SH-SY5Y neuroblastoma cells by a redox-sensitive mechanism
复制标题
DOI：
10.1097/01.wcb.0000090622.86921.0e
复制
发表时间：
2003-11-01
影响因子：
6.3
通讯作者：
Münch, G
中科院分区：
文献类型：
--
作者：
de Arriba, SG;Loske, C;Münch, G
晚期糖基化终产物(AGEs)积聚在长寿蛋白上，包括阿尔茨海默病中的β-淀粉样斑块，并被认为是导致神经元功能障碍和细胞死亡的原因。我们研究了模型年龄对神经母细胞瘤细胞系中葡萄糖代谢和能量产生的影响。AGEs降低细胞内的ATP水平，增加葡萄糖的消耗和乳酸的产生。所有由AGE引起的代谢变化都可以被抗氧化剂如(R+)-α-硫辛酸和17-β-雌二醇所减弱。这些抗氧化剂可能通过对细胞能量代谢的积极作用而成为对抗(年龄介导的)神经退行性变的有效药物。
Advanced glycation endproducts (AGEs) accumulate on long-lived proteins, including beta-amyloid plaques in Alzheimer's disease, and are suggested to contribute to neuronal dysfunction and cell death. We have investigated the effects of a model AGE upon glucose metabolism and energy production in a neuroblastoma cell line. AGEs decrease cellular ATP levels and increase glucose consumption and lactate production. All of the AGE-induced metabolic changes can be attenuated by antioxidants such as (R+)-alpha-lipoic acid and 17beta-estradiol. These antioxidants may become useful drugs against (AGE-mediated) effects in neurodegeneration through their positive effects on cellular energy metabolism.