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  11. Palmatine Inhibits Expression Fat Mass And Obesity Associated Protein (fto) And Exhibits A Curative Effect In Dextran Sulfate Sodium (dss)-induced Experimental Colitis.

Palmatine inhibits expression fat mass and obesity associated protein (FTO) and exhibits a curative effect in dextran sulfate sodium (DSS)-induced experimental colitis.

Wanli Ji1, Yan Huo2, Yifan Zhang1

  • 1School of Pharmacy, Shanghai University of Medicine and Health Sciences, Shanghai 201318, China.

International Immunopharmacology
|April 5, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Palmatine (PAL) effectively treats ulcerative colitis by regulating N6-methyladenosine (m6A) methylation. This natural compound reduces inflammation and repairs the intestinal barrier, offering a promising therapeutic approach for inflammatory bowel disease.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Pharmacology

Background:

  • Ulcerative colitis (UC) is an inflammatory bowel disease with incompletely understood mechanisms.
  • N6-methyladenosine (m6A) methylation is implicated in inflammatory bowel disease (IBD) pathogenesis.
  • Palmatine (PAL), an alkaloid, exhibits anti-inflammatory properties relevant to colitis models.

Purpose of the Study:

  • To investigate the therapeutic role of Palmatine (PAL) in experimental colitis.
  • To elucidate the involvement of m6A methylation in PAL's protective effects against colitis.
  • To examine PAL's impact on key molecular pathways and intestinal barrier function.

Main Methods:

  • Established a rat model of colitis using dextran sulfate sodium (DSS) and treated with PAL.
Keywords:
Experimental colitisFTOPalmatinem6A

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  • Assessed colonic pathology, disease activity index (DAI), and histological damage.
  • Utilized in vitro cell models (NCM460) to evaluate inflammatory markers, intestinal barrier integrity (ZO-1, TEER), and m6A-related protein expression (METTL3, METTL14, ALKBH5, FTO).

    • Main Results:

    • PAL treatment significantly ameliorated colitis symptoms in rats, reducing body weight loss, colon shortening, DAI, and histological damage.
    • PAL inhibited pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8) in both in vivo and in vitro models.
    • PAL enhanced ZO-1 expression and transepithelial electrical resistance (TEER), indicating repair of intestinal barrier dysfunction. It also modulated m6A methylation by increasing METTL3/METTL14 and decreasing FTO/ALKBH5 levels.

    Conclusions:

    • Palmatine demonstrates significant therapeutic efficacy in DSS-induced experimental colitis.
    • PAL's protective effects are linked to the inhibition of FTO expression and the regulation of m6A methylation.
    • These findings highlight PAL as a potential therapeutic agent for ulcerative colitis by targeting m6A modification pathways.