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<p>Ulcerative colitis (UC) constitutes a principal subtype of inflammatory bowel disease (IBD) and exhibits escalating global incidence. This study elucidates the therapeutic efficacy and mechanistic basis of novel selenized probiotic, <i>Lactobacillus brevis</i> 23017 (Se-Lb23017), and biogenic selenium nanoparticles (SeNPs) in a dextran sodium sulfate (DSS)-induced colitis murine model. The investigation specifically probed ferroptosis inhibition and activation of the Nrf2-GPX4-HO-1 signaling axis. The results demonstrated 80&#xa0;µg/mL of Na<sub>2</sub>SeO<sub>3</sub> is optimal for preparing Se-Lb23017. Both Se-Lb23017 and SeNPs exhibited typical morphology under scanning electron microscopy (SEM). In vivo experiments showed that administration of either Se-Lb23017 or SeNPs, especially Se-Lb23017 effectively mitigated key features of colitis, including elevated disease activity index (DAI) scores, weight loss, tissue damage, and colon shortening. In vitro, both Se-Lb23017 and SeNPs, especially Se-Lb23017 significantly reduced the expression of pro-inflammatory mediators (TNF-α, IL-1β, IL-6) and enhanced levels of anti-inflammatory cytokine IL-10. Mechanistically, the protective effects were associated with reduced oxidative stress and ferroptosis suppression via Nrf2-GPX4-HO-1 axis activation and subsequent reduction in lipid peroxidation. Collectively, these findings demonstrate that Se-Lb23017 and SeNPs ameliorate experimental colitis through synergistic anti-inflammatory and antioxidant effects, providing cytoprotection via Nrf2-dependent ferroptosis inhibition. This study highlights selenized probiotics as a promising therapeutic strategy for ulcerative colitis by targeting a novel cell death modality.</p> Graphical Abstract <p></p>

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Selenized Probiotic L. brevis 23017 Alleviates Colitis by Modulating the Nrf2-GPX4 Axis to Inhibit Ferroptosis

  • 期刊论文

  • 发表日期：

    2026年5月7日

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  • Yuxin Zhuang,
  • Qiuju Liu,
  • Fangfei Shi,
  • Rui Kong,
  • Chunli Ma,
  • Dexing Ma

摘要

Ulcerative colitis (UC) constitutes a principal subtype of inflammatory bowel disease (IBD) and exhibits escalating global incidence. This study elucidates the therapeutic efficacy and mechanistic basis of novel selenized probiotic, Lactobacillus brevis 23017 (Se-Lb23017), and biogenic selenium nanoparticles (SeNPs) in a dextran sodium sulfate (DSS)-induced colitis murine model. The investigation specifically probed ferroptosis inhibition and activation of the Nrf2-GPX4-HO-1 signaling axis. The results demonstrated 80 µg/mL of Na2SeO3 is optimal for preparing Se-Lb23017. Both Se-Lb23017 and SeNPs exhibited typical morphology under scanning electron microscopy (SEM). In vivo experiments showed that administration of either Se-Lb23017 or SeNPs, especially Se-Lb23017 effectively mitigated key features of colitis, including elevated disease activity index (DAI) scores, weight loss, tissue damage, and colon shortening. In vitro, both Se-Lb23017 and SeNPs, especially Se-Lb23017 significantly reduced the expression of pro-inflammatory mediators (TNF-α, IL-1β, IL-6) and enhanced levels of anti-inflammatory cytokine IL-10. Mechanistically, the protective effects were associated with reduced oxidative stress and ferroptosis suppression via Nrf2-GPX4-HO-1 axis activation and subsequent reduction in lipid peroxidation. Collectively, these findings demonstrate that Se-Lb23017 and SeNPs ameliorate experimental colitis through synergistic anti-inflammatory and antioxidant effects, providing cytoprotection via Nrf2-dependent ferroptosis inhibition. This study highlights selenized probiotics as a promising therapeutic strategy for ulcerative colitis by targeting a novel cell death modality.

Graphical Abstract