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Peer-reviewedCC BY-NC 4.0Journal of Inflammation Research

Gossypetin Attenuates Concanavalin A-Induced Inflammatory Responses in Macrophages in vitro by Suppressing Oxidative Stress and p38 MAPK/NF-κB Signaling

  • Soyeon Jang1
  • Jiwon Ko2,3
  • Hyejin Hyung4
  • Hee Young Chae2
  • Young Jin Lee2
  • Si-Yong Kim2
  • Su-Geun Lim3
  • Ji Yeong Park2,3
  • Soyoung Jang5
  • Seong-Kyoon Choi3
  • Myoung Ok Kim6
  • Zae Young Ryoo2,6
6 affiliations
  1. 1Institute of Life Science and Biotechnology, Kyungpook National University, Daegu, 41566, Republic of Korea
  2. 2School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Republic of Korea
  3. 3Core Protein Resources Center, DGIST, Daegu, 42988, Republic of Korea
  4. 4Organelle Institute, Kyungpook National University, Daegu, 41566, Republic of Korea
  5. 5Division of Animal Bioscience and Integrated Biotechnology, Gyeongsang National University, Jinju, 52828, Republic of Korea
  6. 6Department of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, 37224, Republic of Korea
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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.

Methods: 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).

Results: 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.

Discussion: 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.

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Cite

BibTeXRIS
BibTeX
@article{jang2026gossypetin,
  title = {{Gossypetin Attenuates Concanavalin A-Induced Inflammatory Responses in Macrophages in vitro by Suppressing Oxidative Stress and p38 MAPK/NF-κB Signaling}},
  author = {Soyeon Jang and Jiwon Ko and Hyejin Hyung and Hee Young Chae and Young Jin Lee and Si-Yong Kim and Su-Geun Lim and Ji Yeong Park and Soyoung Jang and Seong-Kyoon Choi and Myoung Ok Kim and Zae Young Ryoo},
  journal = {Journal of Inflammation Research},
  year = {2026},
  month = nov,
  doi = {10.2147/jir.s646279},
  url = {https://doi.org/10.2147/jir.s646279},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Gossypetin Attenuates Concanavalin A-Induced Inflammatory Responses in Macrophages in vitro by Suppressing Oxidative Stress and p38 MAPK/NF-κB Signaling
AU  - Soyeon Jang
AU  - Jiwon Ko
AU  - Hyejin Hyung
AU  - Hee Young Chae
AU  - Young Jin Lee
AU  - Si-Yong Kim
AU  - Su-Geun Lim
AU  - Ji Yeong Park
AU  - Soyoung Jang
AU  - Seong-Kyoon Choi
AU  - Myoung Ok Kim
AU  - Zae Young Ryoo
PY  - 2026
DA  - 2026/11/05
JO  - Journal of Inflammation Research
DO  - 10.2147/jir.s646279
UR  - https://doi.org/10.2147/jir.s646279
AB  - 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.  Methods: 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).  Results: 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.  Discussion: 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.
SN  - 1178-7031
ER  -