Enhancing Gut Barrier Integrity: Upregulation of Tight Junction Proteins by Chitosan Oligosaccharide through the ERK1/2 Signaling Pathway


Li Y., Wu L., Yong Y., Niu X., Gao Y., Zhou Q., ...More

NUTRITION, vol.124, pp.1-13, 2024 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 124
  • Publication Date: 2024
  • Doi Number: 10.1016/j.nut.2024.112428
  • Journal Name: NUTRITION
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, Aquatic Science & Fisheries Abstracts (ASFA), CAB Abstracts, CINAHL, Food Science & Technology Abstracts, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.1-13
  • Ataturk University Affiliated: Yes

Abstract

Objectives: This study aimed to explore the protective mechanism of chitosan oligosaccharide (COS) against lipopolysaccharide (LPS)-induced inflammatory responses in IEC-6 cells and dextran sodium sulfate (DSS)induced colitis in mice. Methods: The cell inflammation model was constructed by LPS in vitro and enteritis model by DSS in vivo. Results: Following LPS exposure, IEC-6 cell proliferation significantly decreased, epithelial cell integrity was compromised, and TNF- a and IL -1 b levels were increased. However, COS pretreatment reversed these changes. In vivo , DSS-treated mice exhibited evident pathological alterations, including heightened inflammatory levels and significantly decreased expression of tight junction proteins and critical proteins in the Mitogen activated proteins kinase signaling pathway. Nevertheless, COS administration notably reduced inflammatory levels and increased the expression of tight junction proteins and key proteins in the Mitogen activated proteins kinase signaling pathway. Conclusions: Our findings suggest that COS safeguards gut barrier integrity by upregulating tight junction proteins through the ERK1/2 signaling pathway. Therefore, COS has emerged as a promising candidate for novel drug interventions against inflammatory bowel disease. (c) 2024 Elsevier Inc. All rights reserved.