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Prostaglandins Leukot Essent Fatty Acids. 2018 Sep;136:85-94. doi: 10.1016/j.plefa.2017.07.003. Epub 2017 Jul 14.

DHA, EPA and their combination at various ratios differently modulated Aβ25-35-induced neurotoxicity in SH-SY5Y cells.

Author information

1
Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China; Department of Psychology and Neuroscience, Dalhousie University, Halifax B3H 4R2, Canada; Marine Medicine Research and Development Center, Shenzhen Institute of Guangdong Ocean University, Shenzhen 518120, China.
2
Department of Psychology and Neuroscience, Dalhousie University, Halifax B3H 4R2, Canada.
3
Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China; Marine Medicine Research and Development Center, Shenzhen Institute of Guangdong Ocean University, Shenzhen 518120, China.
4
Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China; Department of Psychology and Neuroscience, Dalhousie University, Halifax B3H 4R2, Canada; Marine Medicine Research and Development Center, Shenzhen Institute of Guangdong Ocean University, Shenzhen 518120, China; Graduate Institute of Biomedical Sciences, College of Medicine, China Medical University, Taichung 40402, Taiwan; Departments of Medical Research, China Medical University Hospital, Taichung 40402, Taiwan. Electronic address: cai.song@dal.ca.

Abstract

Omega-3 polyunsaturated fatty acids (n-3 PUFAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), have been reported to prevent neurodegenerative diseases such as Alzheimer's disease (AD) in both experimental and clinical/epidemiological studies. However, whether DHA and EPA from natural products exert similar or different neuroprotective effects and how these n-3 PUFAs target cellular and molecular mechanisms associated with neurodegenerative disease pathogenesis are unknown. In the present study, we used amyloid-β (Aβ)25-35-treated differentiated SH-SY5Y cells as a model of AD to compare the neuroprotective effect of DHA, EPA and their combination at various ratios. Administration of 20μM Aβ25-35 significantly decreased SH-SY5Y cell viability, the expression of nerve growth factor (NGF), its TrkA receptor, and the level of glutathione (GSH) and increased reactive oxygen species (ROS), nitric oxide, tumor necrosis factor (TNF)-α, brain derived neurotrophic factor (BDNF) and its TrkB receptor. Aβ25-35 also increased the Bax/Bcl-2 ratio and the expression of Caspase-3 in these cells. Compared with the Aβ group, pretreatment with DHA/EPA significantly reduced cell death, especially at ratio of 1:1 and 2:1 DHA/EPA or pure DHA. However, the most efficient ratio for reducing changes in ROS and GSH and for decreasing TNF-α appeared at ratio of 1:2 and 1:1, respectively. The ratio of 1:1, 2:1 and pure DHA resulted in significant increase in the level of NGF. Furthermore, pure DHA was the most efficient for reducing Bax/Bcl ratio and Caspase-3 expression. In conclusion, DHA, EPA and their combination differently modulated Aβ25-35-induced neurotoxicity in SH-SY5Y cells by exerting anti-oxidative, anti-inflammatory and neurotrophic effects.

KEYWORDS:

Alzheimer's disease (AD); Aβ(25–35); Human neuroblastoma cell (SH-SY5Y); Neuroprotection; Ratios of DHA/EPA

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