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Atractylenolide-1 Alleviates Ulcerative Colitis via Restraining RhoA/ROCK/MLC Pathway-Mediated Intestinal Barrier

Zengxiang Gao1, Xuecheng Yu1, Wenlong Su1

  • 1College of Pharmacy, Hubei University of Chinese Medicine, Wuhan 430065, People's Republic of China.

Journal of Agricultural and Food Chemistry
|May 14, 2025
PubMed
Summary
This summary is machine-generated.

Atractylenolide-1 (AT-1) effectively treats ulcerative colitis (UC) by restoring the gut barrier and promoting cell repair. This natural compound targets RhoA, improving colon health in disease models.

Keywords:
RhoA/ROCK/MLCatractylenolide-1intestinal barrier dysfunctiontight junctionulcerative colitis

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Area of Science:

  • Pharmacology
  • Gastroenterology
  • Molecular Biology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by gut barrier dysfunction.
  • Current treatments have limitations, necessitating the exploration of novel therapeutic agents.
  • Atractylenolide-1 (AT-1), a natural compound, shows potential for UC treatment.

Purpose of the Study:

  • To investigate the therapeutic effects of AT-1 on dextran sodium sulfate (DSS)-induced ulcerative colitis in mice and Caco-2 cells.
  • To elucidate the molecular mechanisms underlying AT-1's action in restoring mucosal integrity.
  • To identify potential molecular targets of AT-1.

Main Methods:

  • Induction of UC in mice using DSS and assessment of disease parameters (weight loss, DAI, spleen index, histology).
  • Evaluation of AT-1's effects on Caco-2 cell monolayer integrity and F-actin.
  • Molecular docking and dynamics simulations to identify AT-1 targets, focusing on RhoA.
  • Investigation of RhoA interference on AT-1's therapeutic pathway.

Main Results:

  • AT-1 treatment significantly reduced UC symptoms, including weight loss, colon shortening, and inflammation markers.
  • AT-1 restored epithelial cell integrity, F-actin organization, and tight junction protein distribution.
  • AT-1 modulated amino acid metabolism, promoting cell proliferation and restoring the mucosal barrier.
  • Molecular simulations identified RhoA as a stable binding target for AT-1, and its interference abrogated AT-1's effects.

Conclusions:

  • AT-1 demonstrates significant therapeutic potential for ulcerative colitis by ameliorating inflammation and restoring gut barrier function.
  • AT-1 exerts its protective effects by targeting RhoA, influencing cytoskeletal dynamics, amino acid metabolism, and tight junction integrity.
  • AT-1 represents a promising natural therapeutic strategy for managing UC and related gastrointestinal disorders.