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Nitazoxanide protects against experimental ulcerative colitis through improving intestinal barrier and inhibiting

Hu-Tai-Long Zhu1, Jing Luo1, Yi Peng1

  • 1Department of Pharmacology, China Pharmaceutical University, Nanjing, People's Republic of China.

Chemico-Biological Interactions
|April 25, 2024
PubMed

Insights

Nitazoxanide effectively treats ulcerative colitis by improving intestinal barrier function and reducing inflammation. This study reveals its mechanism involves activating AMPK and inhibiting JAK2/STAT3 signaling pathways.

Area of Science:

  • Gastroenterology
  • Immunology
  • Pharmacology

Background:

  • Ulcerative colitis is a chronic inflammatory condition affecting the colon.
  • Nitazoxanide is an antiprotozoal drug with known anti-inflammatory properties.
  • Previous studies suggest nitazoxanide and its metabolite tizoxanide activate AMPK and inhibit inflammation.

Purpose of the Study:

  • To investigate the therapeutic effects of nitazoxanide on dextran sulfate sodium (DSS)-induced colitis in mice.
  • To elucidate the underlying molecular mechanisms of nitazoxanide's action in colitis.

Main Methods:

  • Mice were administered nitazoxanide orally following DSS induction of colitis.
  • Assessed disease activity index (DAI), body weight, colon length, intestinal barrier function, and inflammatory cytokine expression (IL-6, IL-17).
  • Investigated the impact of nitazoxanide and tizoxanide on AMPK, JAK2/STAT3 signaling, CDX2 expression, tight junction proteins (ZO-1, occludin), and macrophage polarization (M2) in vitro and in vivo.

Main Results:

  • Nitazoxanide treatment significantly ameliorated colitis symptoms, including reduced DAI, improved body weight, and shorter colon length.
  • Nitazoxanide improved intestinal barrier function and decreased IL-6 and IL-17 levels in colon tissues.
  • Mechanistically, nitazoxanide/tizoxanide activated AMPK, inhibited JAK2/STAT3 signaling, increased CDX2 and tight junction protein expression, and promoted M2 macrophage polarization.

Conclusions:

  • Nitazoxanide demonstrates protective effects against DSS-induced ulcerative colitis in mice.
  • The therapeutic benefits are attributed to enhanced intestinal barrier integrity and suppressed inflammation.
  • Key mechanisms involve AMPK activation and JAK2/STAT3 pathway inhibition.
Keywords:
AMPKIntestinal barrierMacrophagesNitazoxanideTizoxanideUlcerative colitis

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