Cyanidin-3-glucoside suppresses cytokine-induced inflammatory response in human intestinal cells: comparison with 5-aminosalicylic acid

• Autor(a) principal: Serra, Diana
• Data de Publicação: 2013
• Outros Autores: Paixão, Joana Isabel Félix, Nunes, Carla, Dinis, Teresa C. P., Almeida, Leonor M.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10316/109770; https://doi.org/10.1371/journal.pone.0073001
• topic: Anthocyanins; Anti-Inflammatory Agents; Cell Line; Cell Nucleus; Cell Survival; Cyclooxygenase 2; Cytokines; Dinoprostone; Enzyme Activation; Glucosides; HT29 Cells; Humans; Inflammation; Inflammation Mediators; Inflammatory Bowel Diseases; Interleukin-8; Intestinal Mucosa; Mesalamine; Nitric Oxide; Nitric Oxide Synthase Type II; Phosphorylation; STAT1 Transcription Factor; Transcription Factor RelA; p38 Mitogen-Activated Protein Kinases

The potential use of polyphenols in the prevention and treatment of chronic inflammatory diseases has been extensively investigated although the mechanisms involved in cellular signaling need to be further elucidated. Cyanidin-3-glucoside is a typical anthocyanin of many pigmented fruits and vegetables widespread in the human diet. In the present study, the protection afforded by cyanidin-3-glucoside against cytokine-triggered inflammatory response was evaluated in the human intestinal HT-29 cell line, in comparison with 5-aminosalicylic acid, a well-established anti-inflammatory drug, used in inflammatory bowel disease. For this purpose, some key inflammatory mediators and inflammatory enzymes were examined. Our data showed that cyanidin-3-glucoside reduced cytokine-induced inflammation in intestinal cells, in terms of NO, PGE2 and IL-8 production and of iNOS and COX-2 expressions, at a much lower concentration than 5-aminosalicylic acid, suggesting a higher anti-inflammatory efficiency. Interestingly, cyanidin-3-glucoside and 5-aminosalicylic acid neither prevented IkB-α degradation nor the activation of NF-kB, but significantly reduced cytokine-induced levels of activated STAT1 accumulated in the cell nucleus. In addition, we established that phosphorylated p38 MAPK was not involved in the protective effect of cyanidin-3-glucoside or 5-aminosalicylic acid. Taking into account the high concentrations of dietary anthocyanins potentially reached in the gastrointestinal tract, cyanidin-3-glucoside may be envisaged as a promising nutraceutical giving complementary benefits in the context of inflammatory bowel disease.