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在阿尔茨海默病细胞模型中，番茄红素通过PI3K/Akt/Nrf2信号通路减轻氧化应激。

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

作者信息

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

机构信息

Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.

The 5th Affiliated Hospital, Sun Yat-sen University, Zhuhai, China.

出版信息

PeerJ. 2020 Jun 8;8:e9308. doi: 10.7717/peerj.9308. eCollection 2020.

DOI:10.7717/peerj.9308
PMID:32551202
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7289143/
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 β -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.

摘要

背景与目的

氧化应激（OS）在诸如阿尔茨海默病（AD）等神经退行性疾病中起重要作用。番茄红素是一种具有强大抗氧化和抗肿瘤作用的色素。然而，其在中枢神经系统中的潜在作用尚不明确。本研究旨在探讨番茄红素对AD细胞模型的影响并确定其潜在机制。

方法

M146L细胞是一种双转染（人APP基因和早老素-1基因）的中国仓鼠卵巢（CHO）细胞系，其过表达β-淀粉样蛋白（Aβ），是AD的理想细胞模型。我们用番茄红素处理细胞，并观察番茄红素对M146L细胞的影响。

结果

M146L细胞中的氧化应激和凋亡显著高于CHO细胞，表明Aβ诱导了氧化应激和凋亡。番茄红素减轻了氧化应激和凋亡，激活了PI3K/Akt/Nrf2信号通路，上调了抗氧化和抗凋亡蛋白，下调了促凋亡蛋白。此外，番茄红素抑制了M146L细胞中的β-分泌酶（BACE）活性。这些结果表明，番茄红素通过激活PI3K/Akt/Nrf2途径抑制BACE活性并保护M146L细胞免受氧化应激和凋亡。

结论

番茄红素可能通过激活PI3K/Akt/Nrf2信号通路并降低M146L细胞中BACE的表达来预防Aβ诱导的损伤。

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