The effect of different polyphenols against neurotoxicity induced by quinolinic acid in U87-MG glial cells

• Autor(a) principal: Santos, Júlia Maiara dos
• Data de Publicação: 2022
• Outros Autores: Visentin, Ana Paula Vargas, Scariot, Fernando Joel, Echeverrigaray, Sergio, Salvador, Mirian, Branco, Catia Santos
• Tipo de documento: Artigo
• Idioma: por
• Título da fonte: Research, Society and Development
• Texto Completo: https://rsdjournal.org/index.php/rsd/article/view/24865
• topic: neurodegeneration; Neurodegeneration; quinolinic acid; Quinolinic acid; polyphenols; Polyphenols; oxidative stress; Oxidative stress.; Neurodegeneração; neurodegeneração; ácido quinolínico; Ácido quinolínico; Polifenóis; polifenóis; estresse oxidativo; Estresse oxidativo.; neurodegeneración; Neurodegeneración; ácido quinolínico; Ácido quinolínico; polifenoles; Polifenoles; estrés oxidativo; Estrés oxidativo.

Neurodegenerative disorders (ND) are very debilitating aging-related diseases and mitochondrial dysfunction, oxidative and nitrosative stress (ONS) have been demonstrated to be associated with its clinical manifestations. Mitochondria stand out as crucial organelles in the interplay between neurodegeneration and neuroinflammation, and polyphenols are promising mitochondria-targeting medicine. Phenolic compounds can regulate mitochondria controlling their redox state, function and apoptosis system. In this work, it was investigated the neuroprotective potential of Araucaria angustifolia (AAE) and Camellia sinensis (GT) extracts and six isolated compounds (resveratrol, gallic acid, ellagic acid, catechin, epicatechin and proanthocyanidins) in U87-MG glial cells. Further, the compounds that exhibited the best results were tested in a neurodegeneration model using quinolinic acid (QA). Among phenolic compounds, AAE and GT stood out, and maintained the glial viability around 100%, even in lower doses. Cells exposed to QA presented decreased viability, exacerbated reactive oxygen species (ROS) generation, reduced the mitochondrial membrane potential, and increased inflammatory response. U87-MG glial cells pre-treated with AAE or GT for 1 hour and then exposed to QA for 24 hours were able to prevent all these alterations induced by QA. Despite the similar results found with both GT and AAE, the last one was capable to prevent all the parameters tested in this work. In conclusion, we suggest that AAE could be a potential agent to prevent ND related to mitochondrial dysfunction associated with ONS.