Dietary red raspberries attenuate dextran sulfate sodium-induced acute colitis |
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| Affiliation: | 1. School of Food Science, Washington State University, Pullman, WA 99164, USA;2. Department of Animal Science, Washington State University, Pullman, WA 99164, USA;1. Guelph Research and Development Centre, Agriculture and Agri-Food Canada, Guelph, ON, Canada, N1G 5C9;2. Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, ON, Canada, N1G 2W1;3. Department of Plant Agriculture, University of Guelph, Guelph, ON, Canada, N1G 2W1;4. School of Nutrition Sciences, University of Ottawa;1. School of Food Science, Washington State University, Pullman, Washington, USA;2. Department of Animal Science, Washington State University, Pullman, Washington, USA;3. Tianjin University of Science and Technology, Tianjin, P. R. China;1. School of Food Science, Washington State University, Pullman, WA 99164, USA;2. Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA;1. CIBER-EHD, Department of Pharmacology, ibs. GRANADA, CIBM, University of Granada, Spain;2. School of Food Engineering, University of Campinas, Brazil;3. Department of Nutrition and Bromatology, University of Granada, Spain |
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| Abstract: | Persistent intestinal inflammation severely impairs intestinal integrity resulting in inflammatory bowel disease. Red raspberries (RB) are a rich source of bioactive compounds; their beneficial effect on the colitis protection was evaluated in the current study using a dextran sulfate sodium (DSS)-induced acute colitis mouse model. Six-week-old mice were fed a standard rodent research diet supplemented with RB (0 or 5% w/w, n=20 each group) for 6 weeks. At the 4th week of dietary treatment, approximately half of mice in each dietary group (n=12 each group) were subjected to 2.5% DSS induction for 6 days, followed by 6 days of recovery, to induce colitis. RB supplementation decreased body weight loss (P≤.01), disease activity index (P≤.01), and colon shortening (P≤.05) in DSS-treated mice. In addition, RB supplementation protected the colonic structure (P≤.01), associated with suppressed NF-κB signaling and reduced expression of inflammatory interleukin (IL)-1β, IL-6, IL-17, cyclooxegenase-2, and tumor necrosis factor-α in DSS-treated mice. RB supplementation reduced neutrophil infiltration, monocyte chemoattractant protein-1 mRNA expression, and xanthine oxidase content, but enhanced catalase content in DSS-treated mice. Consistently, RB supplementation reduced pore forming tight junction protein claudin-2, increased barrier strengthening claudin-3, zonula occluden-1 protein content and mucin (MUC)-2 mRNA level, and activated AMP-activated protein kinase (AMPK) in DSS-treated mice. In conclusion, dietary RB protected against inflammation and colitis symptoms induced by DSS, providing a promising dietary approach for the management of colitis. |
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