Preventive and Prebiotic Effect of α-Galacto-Oligosaccharide against Dextran Sodium Sulfate-Induced Colitis and Gut Microbiota Dysbiosis in Mice

• DOI: 10.1021/acs.jafc.1c03792
• Publication Date: 2021-08-11T14:16:59Z
• Authors: Ningning He; Yueyuan Wang; Zihan Zhou; Nian Liu; Samil Jung; Myeong-sok Lee; Shangyong Li
• Keywords: 0301 basic medicine; Chemical Sciences not elsewhere classified; α- GOS treatment; Colon; Immunology; Oligosaccharides; Biochemistry; Microbiology; gut microbiota dysbiosis mice; family member NLRP 3 inflammasome-m.; enzymatic-synthesized α- GOS; Mice; 03 medical and health sciences; UC; dextran sodium sulfate-induced colitis; α- GOS supplement; Genetics; Animals; Gut microbiota analysis; gut microbiota changes; Sulfates; epithelial barrier integrity; β- GOS; Dextran Sulfate; dysfunctional gut microbiota; Cell Biology; Gut Microbiota Dysbiosis; Colitis; Gastrointestinal Microbiome; 3. Good health; Mice, Inbred C57BL; Disease Models, Animal; Prebiotics; Dysbiosis; Biotechnology; Biological Sciences not elsewhere classified

β-Galacto-oligosaccharide (β-GOS) showed great potential in ulcerative colitis (UC) adjuvant therapy. Herein, the preventive and prebiotic effect of enzymatic-synthesized α-linked galacto-oligosaccharide (α-GOS) was investigated in dextran sodium sulfate-induced colitis and gut microbiota dysbiosis mice. Compared with β-GOS, the α-GOS supplement was more effective in improving preventive efficacy, promoting colonic epithelial barrier integrity, and alleviating inflammation cytokines. Moreover, the activation of the NOD-like receptor (NLR) family member NLRP3 inflammasome-mediated inflammation was significantly inhibited by both α-GOS and β-GOS. Gut microbiota analysis showed that α-GOS treatment reshaped the dysfunctional gut microbiota. The subsequent Spearman's correlation coefficient analysis indicated that these gut microbiota changes were significantly correlated with the inflammatory parameters. These results suggested that the enzymatic-synthesized α-GOS is a promising therapeutic agent in UC prevention and adjuvant treatment by maintaining intestinal homeostasis.