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Global analysis of ginsenoside Rg1 protective effects in β-amyloid-treated neuronal cells

  • Shim, Ji Seon (Department of Physiology, School of Medicine, Kyung Hee University) ;
  • Song, Min-Young (Department of Physiology, School of Medicine, Kyung Hee University) ;
  • Yim, Sung-Vin (Department of Clinical Pharmacology, School of Medicine, Kyung Hee University) ;
  • Lee, Seung-Eun (Department of Herbal Crop Research, National Institute of Horticultural & Herbal Science) ;
  • Park, Kang-Sik (Department of Physiology, School of Medicine, Kyung Hee University)
  • Received : 2016.11.15
  • Accepted : 2016.12.05
  • Published : 2017.10.15

Abstract

Background: A number of reports have described the protective effects of ginsenoside Rg1 (Rg1) in Alzheimer's disease (AD). However, the protective mechanisms of Rg1 in AD remain elusive. Methods: To investigate the potential mechanisms of Rg1 in ${\beta}$-amyloid peptide-treated SH-SY5Y cells, a comparative proteomic analysis was performed using stable isotope labeling with amino acids in cell culture combined with nano-LC-MS/MS. Results: We identified a total of 1,149 proteins in three independent experiments. Forty-nine proteins were significantly altered by Rg1 after exposure of the cells to ${\beta}$-amyloid peptides. The protein interaction network analysis showed that these altered proteins were clustered in ribosomal proteins, mitochondria, the actin cytoskeleton, and splicing proteins. Among these proteins, mitochondrial proteins containing HSD17B10, AARS2, TOMM40, VDAC1, COX5A, and NDUFA4 were associated with mitochondrial dysfunction in the pathogenesis of AD. Conclusion: Our results suggest that mitochondrial proteins may be related to the protective mechanisms of Rg1 in AD.

Keywords

References

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