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<p>Inflammatory bowel diseases (IBD) are chronic inflammatory disorders of the digestive tract, and ferulic acid (FA), a phenolic compound with anti-inflammatory activity, has emerged as a promising therapeutic candidate. In this study, we combined bioinformatics analyses with in vitro molecular experiments to elucidate the anti-inflammatory effects and potential mechanisms of FA in IBD. An IBD-like cellular model was established by stimulating human intestinal epithelial NCM460 cells with lipopolysaccharide (LPS), and the effects of FA on inflammatory cytokines were assessed using ELISA, RT-qPCR, and Western blot. Bioinformatics screening identified STAT3 as a potential target associated with FA-mediated anti-inflammatory activity in IBD. We found that FA markedly downregulated inflammatory cytokines, including IL-6 and TNF-α, and further experimental evidence indicated that FA significantly inhibited the phosphorylation of STAT3, JAK1, and JAK2. Docking simulations showed that FA could embed in the STAT3 binding pocket with a moderate docking score. Collectively, these findings support FA as a low-toxicity candidate modulator of JAK/STAT signaling with potential therapeutic relevance to IBD.</p>

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Identification of potential mechanisms of ferulic acid in inflammatory bowel disease through integrated network pharmacology and experimental validation

  • 期刊论文

  • 发表日期：

    2026年2月16日

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  • Ziyue He,
  • Fangyu Meng,
  • Xian Yang,
  • Jun Zeng

摘要

Inflammatory bowel diseases (IBD) are chronic inflammatory disorders of the digestive tract, and ferulic acid (FA), a phenolic compound with anti-inflammatory activity, has emerged as a promising therapeutic candidate. In this study, we combined bioinformatics analyses with in vitro molecular experiments to elucidate the anti-inflammatory effects and potential mechanisms of FA in IBD. An IBD-like cellular model was established by stimulating human intestinal epithelial NCM460 cells with lipopolysaccharide (LPS), and the effects of FA on inflammatory cytokines were assessed using ELISA, RT-qPCR, and Western blot. Bioinformatics screening identified STAT3 as a potential target associated with FA-mediated anti-inflammatory activity in IBD. We found that FA markedly downregulated inflammatory cytokines, including IL-6 and TNF-α, and further experimental evidence indicated that FA significantly inhibited the phosphorylation of STAT3, JAK1, and JAK2. Docking simulations showed that FA could embed in the STAT3 binding pocket with a moderate docking score. Collectively, these findings support FA as a low-toxicity candidate modulator of JAK/STAT signaling with potential therapeutic relevance to IBD.