Chitin derivatives ameliorate DSS-induced ulcerative colitis by changing gut microbiota and restoring intestinal barrier function

Int J Biol Macromol. 2022 Mar 31:202:375-387. doi: 10.1016/j.ijbiomac.2022.01.049. Epub 2022 Jan 19.

Abstract

Chitin derivatives (CDs), including chitosan (CS), chitooligosaccharides (COS), and glucosamine (GlcN), were administrated in dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) mice. UC symptoms such as body weight loss, reduced food intake, and increased disease activity index were relieved (except GlcNL group). CDs (except GlcNL) exerted a strong protective effect on colon length and colonic structure. Treatment with CDs (except GlcNL) increased IL-10 level, reduced levels of IL-1β, IL-6, TNF-α, myeloperoxidase, and inducible nitric oxide synthase, and enhanced expression of tight junction proteins significantly. CDs (except GlcNL) significantly upregulated IκB-α level, and downregulated p65 and p38 phosphory lation and TLR-4 mRNA transcription level, indicating inhibition of TRL-4/NF-κB/MAPK signaling pathway activity. CD treatments increased relative abundance of gut microbiota, modulated its composition, and increased the concentrations of SCFAs. Our findings indicate that CDs exert an ameliorative effect on UC by change of gut microbiota composition and restoration of intestinal barrier function.

Keywords: Chitin derivatives; Gut microbiota; Ulcerative colitis.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Chitin / metabolism
  • Colitis* / metabolism
  • Colitis, Ulcerative* / chemically induced
  • Colitis, Ulcerative* / drug therapy
  • Colitis, Ulcerative* / metabolism
  • Colon
  • Dextran Sulfate / toxicity
  • Disease Models, Animal
  • Gastrointestinal Microbiome*
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / metabolism

Substances

  • Anti-Inflammatory Agents
  • NF-kappa B
  • Chitin
  • Dextran Sulfate