Salvianolic Acid B Inhibits Aβ Generation by Modulating BACE1 Activity in SH-SY5Y-APPsw Cells.
Alzheimer's disease (AD) is a neurodegenerative disease in humans. The accumulation of amyloid-β (Aβ) plays a critical role in the pathogenesis of AD. Previous studies indicated that Salvianolic acid B (SalB) could ameliorate Aβ-induced memory impairment. However, whether SalB could influence the generation of Aβ is unclear. Here, we show that SalB (25, 50, or 100 µM) reduces the generation of Aβ40 and Aβ42 in culture media by decreasing the protein expressions of BACE1 and sAPPβ in SH-SY5Y-APPsw cells. Meanwhile, SalB increases the levels of ADAM10 and sAPPα in the cells. However, SalB has no impact on the protein expressions of APP and PS1. Moreover, SalB attenuates oxidative stress and inhibits the activity of GSK3β, which might be related to the suppression of BACE1 expression and amyloidogenesis. Our study suggests that SalB is a promising therapeutic agent for AD by targeting Aβ generation.
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China. 18825144748@163.com.
Ying
Y
Tang
Department of Stomatology, Affiliated Hospital of Nantong University, Nantong 226361, China. huangdan114@126.com.
Dan
D
Huang
Nantong Tumor Hospital, Nantong 226361, China. zhangmeihuaandcyd@163.com.
Mei-Hua
MH
Zhang
Rugao Changjiang Hospital, Nantong 226532, China. zws238669@163.com.
Wen-Sheng
WS
Zhang
Maternal and Child Health Hospital of Zhoushan, Zhoushan 316000, China. yingying19870722@163.com.
Yu-Xin
YX
Tang
Zhoushan Hospital, Zhoushan 316004, China. shizhengxiang507@163.com.
Zheng-Xiang
ZX
Shi
Guangzhou Hospital of TCM, Guangzhou 510130, China. denglli@126.com.
Li
L
Deng
The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China. zdh@oncology.org.cn.
Dai-Han
DH
Zhou
Biological Resource Center, Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China. luxinyi99612@126.com.
Xin-Yi
XY
Lu
D000544:Alzheimer Disease / Q000188:drug therapy; D053829:Amyloid Precursor Protein Secretases / Q000235:genetics / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D016282:Aspartic Acid Endopeptidases / Q000235:genetics / Q000378:metabolism*; D001572:Benzofurans / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D002460:Cell Line; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006801:Humans; D015394:Molecular Structure; D027561:Salvia miltiorrhiza / Q000737:chemistry; D053630:Depsides
D053829:Amyloid Precursor Protein Secretases; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D016282:Aspartic Acid Endopeptidases; D001572:Benzofurans; C076944:salvianolic acid B; D053630:Depsides; C509280:BACE1 protein, human
Alzheimer’s disease; Aβ generation; BACE1; GSK3β; Salvianolic acid B; oxidative stress