文献类型：期刊文章

作　　者：李雪[1] 白力丹[1] 董雅琼[1] 常青[2] 武睿[2] 章京[2] 杨晓达[1,3]

机构地区：[1]北京大学医学部药学院天然药物及仿生药物国家重点实验室,化学生物学系,北京100191 [2]北京大学医学部基础医学院病理学系,北京100191 [3]国家中医药管理局中药复方解毒重点研究室,北京100027

出　　处：《Journal of Chinese Pharmaceutical Sciences》

基　　金：National Natural Science Foundation of China(Grant No.21571006 and 21271012)

年　　份：2016

卷　　号：25

期　　号：10

起止页码：754-763

语　　种：中文

收录情况：CAB、CAS、CSCD、CSCD2015_2016、DOAJ、EMBASE、IC、JST、SCOPUS、ZGKJHX、普通刊

摘　　要：The Alzheimer＇s disease （AD） is one of the common cognitive disorders in the elderly. AD shares some similar pathological characters with diabetes mellitus （DM）, suggesting potential application of anti-diabetic agents, such as vanadyl complexes, in therapeutic treatment of AD. In the present work, we studied the effects of vanadyl acetylacetonate （VO（acac）2） and cinnamaldehyde （CA） on an AD model based on SH-SY5Y neural cells. The experimental results showed that VO（acac）2 at sub-micromolar concentrations could improve the viability of neural cells with or without increased β-amyloid （Aβ） burden; and the combination of VO（acac）2 and CA showed an additive cell protection effects. Further investigation revealed that for SH-SY5Y neural cells, VO（acac）2 could activate PPART-AMPK signal transduction and inhibit GSK 3β, one of the major kinases for Tau hyperphosphorylation. Meanwhile, CA could correct the abnormal mitochondrial morphology due to Aβ-induced excessive mitochondrial fission, thus restoring/enhancing the mitochondrial function. In addition, both VO（acac）2 and CA decreased intracellular reactive oxygen species （ROS） level and inhibited formation of toxic Aβ oligomers. Overall, VO（acac）2 might work with CA in improving the neural cell viability under the Aβ burden, suggesting application of vanadium metallodrugs in AD treatment.

关 键 词：Alzheimer＇s disease  Β-AMYLOID SH-SY5Y cells  VANADIUM CINNAMALDEHYDE

分 类 号：R749.16]