Biomol Ther.  2021 May;29(3):290-294. 10.4062/biomolther.2020.195.

3’-O-Acetyl-24-Epi-7,8-Didehydrocimigenol-3-O-β-DXylopryranoside Decreases Amyloid Beta Production in Amyloid Precursor Protein-Transfected HeLa Cells

Affiliations
  • 1Department of Integrative Biological Sciences and Industry, Sejong University, Seoul 05006, Republic of Korea
  • 2Natural Product Research Center, Korea Institute of Science and Technology, Gangneung 25451, Republic of Korea
  • 3Division of Bio-Medical Science & Technology, KIST School, Korea University of Science and Technology, Seoul 02792, Republic of Korea
  • 4Department of Pharmacognosy, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City 700000, Vietnam
  • 5College of Pharmacy, Chungnam National University, Daejeon 34134, Republic of Korea

Abstract

Extracellular beta amyloid (Aβ) plaques are the neuropathological hallmarks of Alzheimer’s disease (AD). Accordingly, reducing Aβ levels is considered a promising strategy for AD prevention. 3’-O-acetyl-24-epi-7,8-didehydrocimigenol-3-O-β-D-xylopryranoside significantly decreased the Aβ production and this effect was accompanied with reduced sAPPβ production known as a soluble ectodomain APP fragment through β-secretases in HeLa cells overexpressing amyloid precursor proteins (APPs). This compound also increased the level of sAPPα, which is a proteolytic fragment of APP by α-secretases. In addition, 3’-O-acetyl-24-epi-7,8-didehydrocimigenol-3-O-β-D-xylopryranoside decreased the protein level of β-secretases, but the protein levels of A disintegrin and metalloproteinase (ADAM) family, especially ADAM10 and ADAM17, are increased. Thus, 3’-O-acetyl-24-epi-7,8-didehydrocimigenol-3-O-β-D-xylopryranoside could be useful in the development of AD treatment in the aspect of amyloid pathology.

Keyword

Alzheimer’s disease; Anti-amyloidogenic effect; Secretases
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