Article Publish Status: FREE
Abstract Title:

Lycopene alleviates oxidative stress via the PI3K/Akt/Nrf2pathway in a cell model of Alzheimer's disease.

Abstract Source:

PeerJ. 2020 ;8:e9308. Epub 2020 Jun 8. PMID: 32551202

Abstract Author(s):

Yinchao Fang, Shanshan Ou, Tong Wu, Lingqi Zhou, Hai Tang, Mei Jiang, Jie Xu, Kaihua Guo

Article Affiliation:

Yinchao Fang


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 overexpressesβ -amyloid (Aβ) 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 Aβ 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 β -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 Aβ-induced damage by activating the PI3K/Akt/Nrf2 signaling pathway and reducing the expression of BACE in M146L cells.

Study Type : In Vitro Study

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