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Reduction of Aβ Generation by Schisandrin B through Restraining Beta-Secretase 1 Transcription and Translation

Zeng Li, Xiao-chang Liu, Rui Li, Jun Chang

School of Pharmacy, Anhui Key Laboratory of Bioactivity of Natural Products, Anhui Medical University, Hefei, Anhui, China (mainland)

Med Sci Monit 2018; 24:1219-1224

DOI: 10.12659/MSM.905127

Available online:

Published: 2018-02-28

BACKGROUND: Beta-secretase 1 (BACE1) is a rate-limiting enzyme in the generation of amyloid beta peptides, which are associated with Alzheimer’s disease (AD). It has been reported that Schisandrin B could improve cognitive functions in animal models of AD, but the underlying mechanisms are not completely understood.
MATERIAL AND METHODS: In this research, in order to investigate the effects of Schisandrin B on amyloid-β (Aβ) metabolism and its mechanisms, amyloid precursor protein (APP) and its proteolytic products were determined by enzyme-linked immunosorbent assay (ELISA), western blotting, and RT-PCR after incubation of N2a/Swe cells with Schisandrin B.
RESULTS: The results indicated that Schisandrin B can significantly reduce the level of secretion of Aβ40 and Aβ42 secreted in N2a/Swe cells. Additionally, there was nonsignificant change in APP level after Schisandrin B treatment. Treatment of Schisandrin B dramatically reduced the mRNA and protein expression levels of BACE1. Moreover, Schisandrin B treatment resulted in a reduction of protein level of sAPPβ, an APP fragment cleavage by BACE1.
CONCLUSIONS: These results suggest that Schisandrin B inhibits the transcription and translation of BACE1, suppresses the activity of BACE1, and ultimately attenuates Aβ generation, which provides a novel mechanism for the regulation of Aβ metabolism by Schisandrin B.

Keywords: Alzheimer Disease, Amyloid Precursor Protein Secretases, Neuropharmacology