机构：[1]The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China[2]Department of Stomatology, Affiliated Hospital of Nantong University, Nantong 226361, China[3]Nantong Tumor Hospital, Nantong 226361, China[4]Rugao Changjiang Hospital, Nantong 226532, China[5]Maternal and Child Health Hospital of Zhoushan, Zhoushan 316000, China[6]Zhoushan Hospital, Zhoushan 316004, China[7]Guangzhou Hospital of TCM, Guangzhou 510130, China[8]Biological Resource Center, Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China广东省中医院
Alzheimer's disease (AD) is a neurodegenerative disease in humans. The accumulation of amyloid-beta (A beta) plays a critical role in the pathogenesis of AD. Previous studies indicated that Salvianolic acid B (Sa1B) could ameliorate A beta-induced memory impairment. However, whether Sa1B could influence the generation of A beta is unclear. Here, we show that Sa1B (25, 50, or 100 mu M) reduces the generation of A beta 40 and A beta 42 in culture media by decreasing the protein expressions of BACE1 and sAPP beta in SH-SY5Y-APPsw cells. Meanwhile, Sa1B increases the levels of ADAM10 and sAPP alpha in the cells. However, Sa1B has no impact on the protein expressions of APP and PS1. Moreover, Sa1B attenuates oxidative stress and inhibits the activity of GSK3 beta, which might be related to the suppression of BACE1 expression and amyloidogenesis. Our study suggests that Sa1B is a promising therapeutic agent for AD by targeting A beta generation.
基金：
National Natural Science Foundation of China [81173161]
