{
  "abstract": "Qilian Zhang,1,* Cunyang Hu,2,* Fang Sun,2 Jing Yao21Department of Pathology, People’s Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 271100, People’s Republic of China; 2School of Basic Medicine, Jining Medical University, Jining, Shandong, 272067, People’s Republic of China*These authors contribute equally to this workCorrespondence: Jing Yao, Jining Medical University, 133 Hehua Road, Jining, 272067, People’s Republic of China, Tel/Fax +863616272, Email yjing_87@163.comObjective: Nootkatone (NKT), a natural sesquiterpenoid ketone with anti-inflammatory properties, has unclear effects on ulcerative colitis (UC). This study investigated the protective effect of NKT against dextran sulfate sodium (DSS)-induced UC in mice and its underlying mechanisms.Methods: A UC-mouse model was established by DSS administration in BALB/c mice, along with an in vitro coculture system comprising peritoneal macrophages and colonic epithelial cells. The therapeutic effect of NKT was evaluated by monitoring body weight, fecal characteristics, colon length, disease activity index (DAI), and histopathological changes in the colon tissues. Goblet cells were observed by Alcian Blue-Periodic Acid Schiff (AB-PAS) staining; the expression of the tight junction proteins, occludin and ZO‑1, was detected by Western blotting. Network pharmacology was used to predict potential targets and pathways, while immunohistochemistry and Western blotting helped verify the expression of apoptosis- and inflammation-related proteins. The NKT effect on intestinal epithelial cell migration was analyzed using cell coculture and scratch assays. Flow cytometry was used to assess macrophage polarization.Results: NKT significantly alleviated body weight loss, the increase in DAI scores, mitigated colon shortening and histopathological damage in UC mice, and upregulated the expression of ZO‑1 and occludin in the colon tissues. The CMC‑Na control group exhibited insignificant improvements. Further, Caspase-3 and the TNF pathway were predicted to be key targets, wherein NKT intervention downregulated the pro-apoptotic protein Bax, apoptosis-executioner protein Caspase-3, and the inflammatory factor TNF-α, while increasing the anti-apoptotic protein Bcl-2. In vitro experiments and flow cytometry further revealed that NKT promoted the migration of mouse colonic epithelial cells and selectively suppressed M1 macrophage polarization in vitro, respectively.Conclusion: NKT exerted a significant ameliorative effect on DSS-induced UC in mice, and the underlying mechanism may be related to the enhancement of intestinal mucosal barrier function, inhibition of epithelial cell apoptosis, suppression of M1 macrophage polarization, and regulation of inflammatory pathways.Keywords: nootkatone, ulcerative colitis, network pharmacology, Bax/Bcl‑2/Caspase‑3",
  "abstract_shown": true,
  "affiliations": [
    "Department of Pathology",
    "Basic Medical College"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 4,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Zhang Q"
    },
    {
      "name": "Hu C"
    },
    {
      "affs": [
        1
      ],
      "name": "Sun F"
    },
    {
      "name": "Yao J"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/b8xagh78efgy3.bib",
  "cited_by": 0,
  "doi": null,
  "fulltext_url": "https://www.dovepress.com/ameliorative-effects-and-underlying-molecular-mechanisms-of-nootkatone-peer-reviewed-fulltext-article-JIR",
  "id": "b8xagh78efgy3",
  "issns": [
    "1178-7031"
  ],
  "landing_url": "https://www.dovepress.com/ameliorative-effects-and-underlying-molecular-mechanisms-of-nootkatone-peer-reviewed-fulltext-article-JIR",
  "language": "en",
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "journal",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "lcc",
      "RB1-214"
    ],
    [
      "lcc",
      "RM1-950"
    ]
  ],
  "openalex": null,
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-01",
  "publisher": "Dove Medical Press",
  "ris": "https://research.draconitic.com/paper/b8xagh78efgy3.ris",
  "sources": [
    {
      "first_seen": "2026-11-02T14:20:53Z",
      "native_id": "1155538d251542e1bce4e12b19caae5c",
      "source": "doaj",
      "url": "https://www.dovepress.com/ameliorative-effects-and-underlying-molecular-mechanisms-of-nootkatone-peer-reviewed-fulltext-article-JIR"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "lcc:RM1-950",
      "subfield": "pharmacology-toxicology"
    }
  ],
  "title": "Ameliorative Effects and Underlying Molecular Mechanisms of Nootkatone in DSS-Induced Ulcerative Colitis in Mice",
  "title_text": "Ameliorative Effects and Underlying Molecular Mechanisms of Nootkatone in DSS-Induced Ulcerative Colitis in Mice",
  "type": "peer-reviewed",
  "updated_at": "2026-11-03T14:20:55Z",
  "url": "https://research.draconitic.com/paper/b8xagh78efgy3",
  "venue": "Journal of Inflammation Research",
  "versions": []
}