Cyanidin-3-O-glucoside modulates intracellular redox status and inflammation induced by LPS in Caco-2 intestinal cells through activation of Nrf2 pathway Ferrari D, Fratantonio D, Cristani M, Saija A, Cimino F, Speciale A Dipartimento di Scienze del Farmaco e dei Prodotti per la Salute - University of Messina, Viale Annunziata, 98168 Messina, Italy Inflammatory bowel diseases (IBDs), the collective name for Crohn’s disease and ulcerative colitis, are characterized by persistent and unpredictable attacks of inflammation of the intestine, causing weight loss, diarrhoea, rectal bleeding, abdominal pain, fever and anemia (Cao et al, 2013). Recent studies support beneficial effects of flavonoids against various chronic inflammatory diseases. Among these compounds, anthocyanins, that are widely distributed in mediterranean diet, have been demonstrated to inhibit NF-kB proinflammatory pathway as protective mechanism in many cell lines. In this study, we employed an in vitro model of the acute phase of intestinal inflammation using Caco-2 cells, a continuous line of heterogeneous human epithelial colorectal adenocarcinoma cells, exposed to lipopolysaccharide (LPS). LPS, in fact, was found to promote gut-barrier dysfunction through an oxidative mechanism and increased epithelial permeability (Hirotani et al, 2008). We then investigated the potential beneficial effects of cyanidin-3-O-glucoside (C3G), the main anthocyanin found in red fruit and vegetables. Caco-2 cells exposure to LPS for 6 h induced an alteration of cellular redox state (increased ROS production), activated NF-kB proinflammatory pathway (p65 nuclear localization) and altered Caco-2 cells barrier permeability. Interestingly, cells pretreatment for 24h with C3G (20 µM) was effective in preventing LPS-induced oxidative stress, and attenuated permeability changes. We have also demonstrated that, C3G avoided LPS-induced p65 nuclear translocation through the involvement of a cellular adaptive response modulated by redox sensitive Nrf2 transcription factor. Finally, our data suggest that C3G may have protective effects against LPS-mediated intestinal mucosal damage and impairment barrier function in intestinal epithelial cells.

Cyanidin-3-O-glucoside modulates intracellular redox status and inflammation induced by LPS in Caco-2 intestinal cells through activation of Nrf-2 Pathway

FRATANTONIO, DEBORAH;
2014

Abstract

Cyanidin-3-O-glucoside modulates intracellular redox status and inflammation induced by LPS in Caco-2 intestinal cells through activation of Nrf2 pathway Ferrari D, Fratantonio D, Cristani M, Saija A, Cimino F, Speciale A Dipartimento di Scienze del Farmaco e dei Prodotti per la Salute - University of Messina, Viale Annunziata, 98168 Messina, Italy Inflammatory bowel diseases (IBDs), the collective name for Crohn’s disease and ulcerative colitis, are characterized by persistent and unpredictable attacks of inflammation of the intestine, causing weight loss, diarrhoea, rectal bleeding, abdominal pain, fever and anemia (Cao et al, 2013). Recent studies support beneficial effects of flavonoids against various chronic inflammatory diseases. Among these compounds, anthocyanins, that are widely distributed in mediterranean diet, have been demonstrated to inhibit NF-kB proinflammatory pathway as protective mechanism in many cell lines. In this study, we employed an in vitro model of the acute phase of intestinal inflammation using Caco-2 cells, a continuous line of heterogeneous human epithelial colorectal adenocarcinoma cells, exposed to lipopolysaccharide (LPS). LPS, in fact, was found to promote gut-barrier dysfunction through an oxidative mechanism and increased epithelial permeability (Hirotani et al, 2008). We then investigated the potential beneficial effects of cyanidin-3-O-glucoside (C3G), the main anthocyanin found in red fruit and vegetables. Caco-2 cells exposure to LPS for 6 h induced an alteration of cellular redox state (increased ROS production), activated NF-kB proinflammatory pathway (p65 nuclear localization) and altered Caco-2 cells barrier permeability. Interestingly, cells pretreatment for 24h with C3G (20 µM) was effective in preventing LPS-induced oxidative stress, and attenuated permeability changes. We have also demonstrated that, C3G avoided LPS-induced p65 nuclear translocation through the involvement of a cellular adaptive response modulated by redox sensitive Nrf2 transcription factor. Finally, our data suggest that C3G may have protective effects against LPS-mediated intestinal mucosal damage and impairment barrier function in intestinal epithelial cells.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/20.500.12572/7552
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