Role of amber extract in protecting SHSY5Y cells against amyloid β1-42-induced neurotoxicity

被引:1
|
作者
Luo, Yuening [1 ]
Zhou, Siqi [1 ]
Haeiwa, Haruna [2 ]
Takeda, Reiko [1 ,2 ]
Okazaki, Kazuma [2 ]
Sekita, Marie [2 ]
Yamamoto, Takuya [1 ,2 ]
Yamano, Mikio [2 ]
Sakamoto, Kazuichi [1 ]
机构
[1] Univ Tsukuba, Grad Sch Life & Environm Sci, Tsukuba, Ibaraki 3058572, Japan
[2] Kohaku Biotechnol Co Ltd, Tsukuba, Ibaraki 3058572, Japan
关键词
Alzheimer disease; Amyloid-beta (1-42); Amber; BACE1; Autophagy; ALZHEIMERS-DISEASE; BETA; APOPTOSIS; PROTEIN; TENUIFOLIN; AUTOPHAGY; MEDICINE; PEPTIDE;
D O I
10.1016/j.biopha.2021.11.1804
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Alzheimer disease (AD) is an irreversible, progressive brain disease. Amyloid beta plays a critical role in AD development. Some Chinese traditional medicines, such as the fossilized plant resin, amber, have been applied as mental stabilizers. However, the effects of amber on AD pathogenesis remain unknown. Therefore, we aimed to determine the potential of amber extract for treating AD by evaluating its effects on amyloid-beta (1-42) (A beta (1-42))-induced neuronal cell death. We measured levels of ROS, Bel-2, and Bax mRNA, and found that amber extract decreased A beta (1-42)-induced cell apoptosis via the reactive oxygen species (ROS)-mediated mitochondrial pathway. Amber extract also decreased beta -site amyloid precursor protein cleaving enzyme 1 (BACE1) and increased microtubule-associated proteins 1A/1B light chain 3B (LC3II) and Beclin 1. These findings suggested that amber extract protects neuronal cells against A beta (1-42)-induced cell apoptosis by upregulating autophagy and downregulating BACE1.
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页数:8
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