Apple polysaccharide protects ICR mice against colitis associated colorectal cancer through the regulation of microbial dysbiosis. (15th February 2020)

• Record Type: Journal Article
• Authors: Li, Yuhua; Wang, Sheng; Sun, Yang; Xu, Wenqi; Zheng, Hongnan; Wang, Yan; Tang, Yuan; Gao, Xiaowei; Song, Can; Long, Yin; Liu, Jiayun; Liu, Li; Mei, Qibing
• Is Part Of: Carbohydrate polymers. Volume 230(2020)
• Publication Date: 2020-02-15
• Subjects: AOM Azoxymethane -- Bde Bacteroides -- Bte Bacteroidetes -- CACC Colitis associated colorectal cancer -- DSS Dextran sodium sulfate -- Fus Fusobacterium -- ICR Institute of cancer research -- Lac Lactobacillus -- LPS Lipopolysaccharide -- AP Apple polysaccharide; Apple polysaccharide -- Colitis associated colorectal cancer -- Bacteria; Polysaccharides -- Periodicals; Polysaccharides -- Periodicals; Polysaccharides -- Périodiques; Electronic journals; 547.78
• DOI: 10.1016/j.carbpol.2019.115726
• Languages: English
• ISSNs: 0144-8617

Abstract

Highlights: Apple polysaccharide (AP) prevented from colitis associated colorectal cancer. AP restored AOM/DSS-caused intestinal microbiota disorder. AP inhibited the activation of classical Wnt pathway in colon tissues. AP decreased the quantity of Fusobacterium directly and/or indirectly. Abstract: The study tried to investigate whether apple polysaccharide (AP) could prevent colitis associated colorectal cancer (CACC) through the regulation of intestinal microbiota disorders. 10 % AP (w/v) was administrated to ICR mice by gavage for 15 wk. It was found that AP treatment protected against CACC in mice effectively. The level of Lactobacillus in the intestine of AOM/DSS-treated mice was significantly decreased and that of Fusobacterium increased; while AP could reverse this trend and increase the intestinal microbiota diversity. The number of T cells and macrophages in the colon tissue of mice in AOM/DSS group elevated; while AP could reduce the number of these cells significantly. AP suppressed nuclear aggregation of β-catenin, inhibited the activation of Wnt pathway in colon tissues. These data suggest that AP prevented ICR mice from CACC at least in part through regulating intestinal flora disorder and Wnt pathway.