Understanding the protective effects of wine components and their metabolites in the brain functionEsteban-Fernández, A., Gigorro del Coso, D., González de Llano, D., Spencer, J. ORCID: https://orcid.org/0000-0003-2931-7274, Bartolomé, B. and Moreno-Arribas, M. V. (2016) Understanding the protective effects of wine components and their metabolites in the brain function. In: 39th World Congress of Vine and Wine, 23 - 28 Oct 2016, Bento Gonçalves, Brazil, 04008, https://doi.org/10.1051/bioconf/20160704008.
It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing. To link to this item DOI: 10.1051/bioconf/20160704008 Abstract/SummaryModerate 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 over MAPK 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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