{
  "abstract": "Introduction: Excessive macrophage activation and oxidative stress contribute to inflammatory disease by sustaining pro-inflammatory signaling. Gossypetin, a naturally occurring hexahydroxyflavone with antioxidant and kinase-modulatory activities, may be particularly relevant to macrophage-mediated inflammation because oxidative stress and MAPK/NF-κB signaling are central regulators of macrophage activation. However, its mechanisms in macrophage-mediated inflammation remain incompletely understood. This study investigated the anti-inflammatory effects and underlying mechanisms of gossypetin in concanavalin A (ConA)-stimulated macrophages.\n\nMethods: RAW264.7 macrophages were stimulated with ConA with or without gossypetin pretreatment. Oxidative stress, mitochondrial membrane potential, MAPK and NF-κB signaling, inflammatory mediator expression, cytokine production, and autophagy-associated changes were evaluated. Pharmacological inhibitors were used to examine the involvement of p38 MAPK, NF-κB, and autophagy-related processes. Key findings were validated in primary bone marrow-derived macrophages (BMDMs).\n\nResults: ConA increased intracellular and mitochondrial reactive oxygen species production, activated MAPK and NF-κB signaling, enhanced COX-2 and iNOS expression, and increased TNF-α and IL-6 production. Gossypetin attenuated oxidative stress, restored mitochondrial membrane potential, suppressed p38 MAPK/NF-κB signaling, and reduced inflammatory mediator expression and cytokine production. Pharmacological inhibition of p38 or NF-κB produced effects consistent with those of gossypetin. Autophagy-associated modulation also appeared to contribute partially to the anti-inflammatory response. These effects were reproduced in primary BMDMs.\n\nDiscussion: Gossypetin attenuates ConA-induced macrophage inflammatory responses in vitro, primarily through suppression of oxidative stress and p38 MAPK/NF-κB signaling. Autophagy-associated regulation may additionally contribute to these effects.",
  "abstract_shown": true,
  "affiliations": [
    "Institute of Life Science and Biotechnology, Kyungpook National University, Daegu, 41566, Republic of Korea",
    "School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Republic of Korea",
    "Core Protein Resources Center, DGIST, Daegu, 42988, Republic of Korea",
    "Organelle Institute, Kyungpook National University, Daegu, 41566, Republic of Korea",
    "Division of Animal Bioscience and Integrated Biotechnology, Gyeongsang National University, Jinju, 52828, Republic of Korea",
    "Department of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, 37224, Republic of Korea"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 12,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Soyeon Jang",
      "orcid": "0009-0002-1118-3781"
    },
    {
      "affs": [
        1,
        2
      ],
      "name": "Jiwon Ko",
      "orcid": "0000-0003-2034-6730"
    },
    {
      "affs": [
        3
      ],
      "name": "Hyejin Hyung",
      "orcid": "0009-0009-9749-2542"
    },
    {
      "affs": [
        1
      ],
      "name": "Hee Young Chae",
      "orcid": "0009-0001-1919-2474"
    },
    {
      "affs": [
        1
      ],
      "name": "Young Jin Lee"
    },
    {
      "affs": [
        1
      ],
      "name": "Si-Yong Kim"
    },
    {
      "affs": [
        2
      ],
      "name": "Su-Geun Lim"
    },
    {
      "affs": [
        1,
        2
      ],
      "name": "Ji Yeong Park"
    },
    {
      "affs": [
        4
      ],
      "name": "Soyoung Jang",
      "orcid": "0000-0003-2673-4259"
    },
    {
      "affs": [
        2
      ],
      "name": "Seong-Kyoon Choi",
      "orcid": "0000-0002-0233-4114"
    },
    {
      "affs": [
        5
      ],
      "name": "Myoung Ok Kim"
    },
    {
      "affs": [
        1,
        5
      ],
      "name": "Zae Young Ryoo",
      "orcid": "0000-0001-6993-3624"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/112vsb8zfmwb7.bib",
  "cited_by": 0,
  "doi": "10.2147/jir.s646279",
  "fulltext_url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC13746900/",
  "id": "112vsb8zfmwb7",
  "issns": [
    "1178-7031"
  ],
  "landing_url": "https://doi.org/10.2147/jir.s646279",
  "language": "en",
  "licence": "CC-BY-NC-4.0",
  "licence_label": "CC BY-NC 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Original Research"
    ],
    [
      "openalex",
      "2736|Flavonoids in Medical Research"
    ]
  ],
  "openalex": "W7225224543",
  "pdf_url": "https://www.dovepress.com/article/download/121882",
  "pmcid": "PMC13746900",
  "pmid": "43005913",
  "published": "2026-11-05",
  "publisher": "Dove Press",
  "ris": "https://research.draconitic.com/paper/112vsb8zfmwb7.ris",
  "sources": [
    {
      "first_seen": "2026-11-11T12:24:12Z",
      "native_id": "PMC13746900",
      "source": "pmc",
      "url": "https://doi.org/10.2147/jir.s646279"
    },
    {
      "first_seen": "2026-11-12T15:21:47Z",
      "native_id": "MED:43005913",
      "source": "europepmc",
      "url": "https://europepmc.org/article/MED/43005913"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2736|Flavonoids in Medical Research",
      "subfield": "pharmacology-toxicology"
    }
  ],
  "title": "Gossypetin Attenuates Concanavalin A-Induced Inflammatory Responses in Macrophages in vitro by Suppressing Oxidative Stress and p38 MAPK/NF-κB Signaling",
  "title_text": "Gossypetin Attenuates Concanavalin A-Induced Inflammatory Responses in Macrophages in vitro by Suppressing Oxidative Stress and p38 MAPK/NF-κB Signaling",
  "type": "peer-reviewed",
  "updated_at": "2026-11-13T12:23:37Z",
  "url": "https://research.draconitic.com/paper/112vsb8zfmwb7",
  "venue": "Journal of Inflammation Research",
  "versions": []
}