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Journal of Chinese Pharmaceutical Sciences ›› 2016, Vol. 25 ›› Issue (10): 754-763.DOI: 10.5246/jcps.2016.10.084

• Original articles • Previous Articles     Next Articles

Vanadyl complexes work with cinnamaldehyde in promoting cell viability under the β­amyloid burden in SH­SY5Y neural cells

Xue Li1, Lidan Bai1, Yaqiong Dong1, Qing Chang2, Rui Wu2, Jing Zhang2*, Xiaoda Yang1,3*   

  1. 1. State Key Laboratories of Natural and Biomimetic Drugs; Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China
    2. Department of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China
    3. SATCM Key Laboratory of Compound Drug Detoxication at Peking University, Beijing 100027, China
  • Received:2016-05-18 Revised:2016-06-10 Online:2016-10-27 Published:2016-06-23
  • Contact: Tel.: +86-010-82805611, E-mail: xyang@bjmu.edu.cn, zhangjing6202@163.com
  • Supported by:
    National Natural Science Foundation of China (Grant No. 21571006 and 21271012).

Abstract:

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 β­amyloid (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 PPARγ-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.

Key words: Alzheimer’s disease, β­Amyloid, SH-SY5Y cells, Vanadium, Cinnamaldehyde

CLC Number: 

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