期刊
NEUROSCIENCE LETTERS
卷 608, 期 -, 页码 28-33出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2015.10.009
关键词
Alzheimer disease; Lycopene; A beta(1-42); APP; Caenorhabditis elegans
资金
- Ministry of Health of Guangxi Province, China [Z2012419]
- Natural Science Foundation of Guangxi Province, China [2013GXNSFAA019132]
- NIH Office of Research Infrastructure Programs [P40 OD010440]
Growing evidence suggests concentration of lycopene was reduced in plasma of patients with Alzheimer disease (AD). Lycopene, a member of the carotenoid family, has been identified as an antioxidant to attenuate oxidative damage and has neuroprotective role in several AD models. However, whether lycopene is involved in the pathogenesis of AD and molecular underpinnings are elusive. In this study, we found that lycopene can significantly delay paralysis in the A beta(1-42)-transgenic Caenorhabditis elegans strain GMC101. Lycopene treatment reduced A beta(1-42) secretion in SH-SY5Y cells overexpressing the Swedish mutant form of human P-amyloid precursor protein (APPsw). Next, we found lycopene can down-regulate expression level of P-amyloid precursor protein(APP) in APPsw cells. Moreover, lycopene treatment can not change endogenous reactive oxygen species level and apoptosis in APPsw cells. However, lycopene treatment protected against H2O2-induced oxidative stress and copper-induced damage in APPsw cells. Collectively, our data support that elevated lycopene contributes to the lower pathogenesis of AD. Our findings suggest that increasing lycopene in neurons may be a novel approach to attenuate onset and development of AD. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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