Lycopene alleviates oxidative stress via the PI3K/Akt/Nrf2pathway in a cell model of Alzheimer's disease.
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ABSTRACT: Background & Aims:Oxidative stress (OS) plays an important role in neurodegenerative diseases such as Alzheimer's disease (AD). Lycopene is a pigment with potent antioxidant and anti-tumor effects. However, its potential role in central nervous system is not well-defined. The aim of this study was to investigate the effect of lycopene on the cell model of AD and determine its underlying mechanisms. Methods:M146L cell is a double-transfected (human APP gene and presenlin-1 gene) Chinese hamster ovary (CHO) cell line that overexpresses ? -amyloid (A?) and is an ideal cell model for AD. We treated cells with lycopene, and observed the effect of lycopene on M146L cells. Results:Oxidative stress and apoptosis in M146L cells were significantly higher than those in CHO cells, suggesting that A? induced OS and apoptosis. Lycopene alleviated OS and apoptosis, activated the PI3K/Akt/Nrf2 signaling pathway, upregulated antioxidant and antiapoptotic proteins and downregulated proapoptotic proteins. Additionally, lycopene inhibited ? -secretase (BACE) activity in M146L cells. These results suggest that lycopene inhibits BACE activity and protects M146L cells from oxidative stress and apoptosis by activating the PI3K/Akt/Nrf2 pathway. Conclusion:Lycopene possibly prevents A?-induced damage by activating the PI3K/Akt/Nrf2 signaling pathway and reducing the expression of BACE in M146L cells.
SUBMITTER: Fang Y
PROVIDER: S-EPMC7289143 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
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