Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0606920210290030290
Biomolecules & Therapeutics
2021 Volume.29 No. 3 p.290 ~ p.294
3¡¯-O-Acetyl-24-Epi-7,8-Didehydrocimigenol-3-O-¥â-DXylopryranoside Decreases Amyloid Beta Production in Amyloid Precursor Protein-Transfected HeLa Cells
Lee Sang-Bin

Park An-Sun
Ma Chi Thanh
Kim Young-Ho
Yang Hyun-Ok
Abstract
Extracellular beta amyloid (A¥â) plaques are the neuropathological hallmarks of Alzheimer¡¯s disease (AD). Accordingly, reducing A¥â levels is considered a promising strategy for AD prevention. 3¡¯-O-acetyl-24-epi-7,8-didehydrocimigenol-3-O-¥â-D-xylopryranoside significantly decreased the A¥â production and this effect was accompanied with reduced sAPP¥â production known as a soluble ectodomain APP fragment through ¥â-secretases in HeLa cells overexpressing amyloid precursor proteins (APPs). This compound also increased the level of sAPP¥á, which is a proteolytic fragment of APP by ¥á-secretases. In addition, 3¡¯-O-acetyl-24-epi-7,8-didehydrocimigenol-3-O-¥â-D-xylopryranoside decreased the protein level of ¥â-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-¥â-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
FullTexts / Linksout information
Listed journal information
SCI(E) ÇмúÁøÈïÀç´Ü(KCI) KoreaMed