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  11. Tetrastigma Hemsleyanum Polysaccharide Ameliorated Ulcerative Colitis By Remodeling Intestinal Mucosal Barrier Function Via Regulating The Socs1/jak2/stat3 Pathway

Tetrastigma hemsleyanum polysaccharide ameliorated ulcerative colitis by remodeling intestinal mucosal barrier function via regulating the SOCS1/JAK2/STAT3 pathway

Xiaodan Bao1, Youying Tang1, Yishan Lv1

  • 1School of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, China.

International Immunopharmacology
|June 8, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Tetrastigma hemsleyanum polysaccharide (THP) shows promise for ulcerative colitis (UC) treatment by restoring gut health and reducing inflammation. THP effectively modulates key inflammatory pathways and improves the intestinal barrier function in UC mouse models.

Area of Science:

  • Gastroenterology
  • Immunology
  • Pharmacology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease with limited treatment options and frequent complications.
  • The therapeutic potential of Tetrastigma hemsleyanum polysaccharide (THP) for inflammatory bowel disease is recognized, but its mechanism in UC is not fully understood.

Purpose of the Study:

  • To investigate the therapeutic effects of THP on dextran sulfate-induced ulcerative colitis (UC) in mice.
  • To elucidate the underlying molecular mechanisms of THP in treating UC.

Main Methods:

  • Induction of UC in mice using dextran sulfate sodium (DSS).
  • Administration of THP and assessment of colon and spleen.
  • Measurement of inflammatory markers, immune cells, tight junction proteins, and gut microbiota.
Keywords:
Intestinal mucosal barrier functionJAK/STAT pathwayTetrastigma hemsleyanum polysaccharideUlcerative colitis

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  • Analysis of signaling pathways including SOCS1/JAK2/STAT3.

    • Main Results:

    • THP treatment restored colon and spleen morphology, increased protective markers (sIgA, β-defensin, MUC2), and decreased collagen deposition and apoptosis.
    • THP enhanced intestinal barrier function by increasing Ki67 and tight junction proteins, reducing permeability, and rebalancing gut microbiota.
    • THP downregulated pro-inflammatory cytokines (IL-6, TNF-α, IL-17) and upregulated regulatory factors (FoxP3, SOCS1), while inhibiting the JAK2/STAT3 pathway.

    Conclusions:

    • THP demonstrates significant efficacy in treating experimental UC, comparable to JAK inhibitors.
    • THP exerts its therapeutic effects by modulating the SOCS1/JAK2/STAT3 signaling pathway and reinforcing the intestinal mucosal barrier.
    • THP represents a potential novel therapeutic agent for ulcerative colitis management.