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<p>The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a multiprotein complex that plays a crucial role in the innate immune system by responding to microbial infections and cellular damage. However, its dysregulated activation is implicated in the development and progression of metabolic diseases, including cryopyrin-associated periodic syndrome, Alzheimer’s disease, type 2 diabetes mellitus, inflammatory bowel disease, obesity, atherosclerosis, and cardiovascular disease. Ginsenosides, the bioactive components of <i>Panax ginseng</i>, have demonstrated significant pharmacological effects on various human diseases. Recently, ginsenosides have garnered attention as potential therapeutic agents for modulating NLRP3 inflammasome activation. In this review, we systematically summarized the progress made in understanding how ginsenosides prevent inflammation and metabolic disorders by targeting the NLRP3 inflammasome. We discussed the molecular mechanisms through which ginsenosides regulate NLRP3 inflammasome activation, with a particular focus on their roles in the two signaling stages of activation. In addition, we described multiple regulatory pathways involving post-translational modifications and intracellular inflammatory cascades. Our objective is to provide novel insights into strategies for preventing and treating NLRP3 inflammasome-related diseases, as well as to highlight opportunities for further research and preclinical evidence supporting their application.</p> Graphical abstract <p></p>

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The potential of ginsenosides from Panax ginseng against the NLRP3 inflammasome

  • 期刊论文

  • 发表日期：

    2025年5月7日

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  • Yanan Liu,
  • Chaoqing Huang,
  • Yujing Feng,
  • Jianmei Zhang,
  • Zhiqiang Niu,
  • Luyao Qi,
  • Ting Shen,
  • Xinyue Gao,
  • Weicheng Hu

摘要

The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a multiprotein complex that plays a crucial role in the innate immune system by responding to microbial infections and cellular damage. However, its dysregulated activation is implicated in the development and progression of metabolic diseases, including cryopyrin-associated periodic syndrome, Alzheimer’s disease, type 2 diabetes mellitus, inflammatory bowel disease, obesity, atherosclerosis, and cardiovascular disease. Ginsenosides, the bioactive components of Panax ginseng, have demonstrated significant pharmacological effects on various human diseases. Recently, ginsenosides have garnered attention as potential therapeutic agents for modulating NLRP3 inflammasome activation. In this review, we systematically summarized the progress made in understanding how ginsenosides prevent inflammation and metabolic disorders by targeting the NLRP3 inflammasome. We discussed the molecular mechanisms through which ginsenosides regulate NLRP3 inflammasome activation, with a particular focus on their roles in the two signaling stages of activation. In addition, we described multiple regulatory pathways involving post-translational modifications and intracellular inflammatory cascades. Our objective is to provide novel insights into strategies for preventing and treating NLRP3 inflammasome-related diseases, as well as to highlight opportunities for further research and preclinical evidence supporting their application.

Graphical abstract