Understanding the protective effects of wine components and their metabolites in the brain function

被引:0
作者
Esteban-Fernandez, A. [1 ]
Gigorro del Coso, D. [1 ]
Gonzalez de Llano, D. [1 ]
Spencer, J. [2 ]
Bartolome, B. [1 ]
Moreno-Arribas, M. V. [1 ]
机构
[1] CSIC UAM, Inst Invest Ciencias Alimentac CIAL, Nicolas Cabrera 9, Madrid 28049, Spain
[2] Univ Reading, Sch Chem Food & Pharm, Dept Food & Nutr Sci, Whiteknights Campus, Reading RG6 6AP, Berks, England
来源
39TH WORLD CONGRESS OF VINE AND WINE | 2016年 / 7卷
关键词
INDUCED APOPTOSIS; MOUSE MODEL; CONSUMPTION; FLAVONOIDS; PEROXYNITRITE; MECHANISMS; MICROBIOTA; DEMENTIA; PATHWAY; STRESS;
D O I
10.1051/bioconf/20160704008
中图分类号
F3 [农业经济];
学科分类号
0202 ; 020205 ; 1203 ;
摘要
Moderate wine consumption has been suggested to exert a positive effect in prevention of neurodegenerative process and cognitive impairment. With the ultimate aim of achieving a better understanding of the molecular mechanisms behind this benefit, we have investigated the role of certain wine-derived phenolic metabolites and aroma compounds in the MAPK cascade (including ERK1/2, p38), one of the routes directly related to inflammation in neuronal cells. Some of the tested phenolic compounds, especially in the case of 3,4-dihydroxyphenylacetic acid, showed a significant neuroprotective effect against SIN-1-induced neuronal death. Regarding their effect overMAPK phosphorylation, inmunoblotting technique revealed a beneficial and significant decrease on the phosphorylation of p38 and ERK1/2 kinases after incubation with wine constituents. In addition, activity of caspase3-like protease, an executor of neuronal apoptosis and a downstream signal of MAPK, was significantly diminished by 3-(3-hydroxyphenyl) propionic acid and linalool, counterbalancing the increase produced by SIN-1. Altogether, these results suggest that wine aroma, phenolic compounds and their gut metabolites could exert neuroprotective actions by modulating MAPK signalling and caspase-3 proteases activation, which are known to play a key role in oxidative/nitrosative stress-induced response.
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页数:4
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