3’-O-Acetyl-24-Epi-7,8-Didehydrocimigenol-3-O-β-DXylopryranoside Decreases Amyloid Beta Production in Amyloid Precursor Protein-Transfected HeLa Cells
10.4062/biomolther.2020.195
- Author:
Sang-Bin LEE
1
;
Ansun PARK
;
Chi Thanh MA
;
Young Ho KIM
;
Hyun Ok YANG
Author Information
1. Department of Integrative Biological Sciences and Industry, Sejong University, Seoul 05006, Republic of Korea
- Publication Type:Original Article
- From:Biomolecules & Therapeutics
2021;29(3):290-294
- CountryRepublic of Korea
- Language:English
-
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 ofA 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.
