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Peer-reviewedCC BYChinese herbal medicines

Parthenolide ameliorated gout-like inflammation by inhibiting activation of NLRP3 inflammasome.

  • Yonghong Cheng1,2
  • Yinjing Jiang1,2
  • Hui Wang1,2
  • Haoqing Zhu1,2
  • Yanling Wu1,2
  • Jixing Nan1,2
  • Lihua Lian1,2
  1. 1Key Laboratory of Traditional Chinese Korean Medicine Research of State Ethnic Affairs Commission, College of Pharmacy, Yanbian University, Yanji 133002, China.
  2. 2Key Laboratory of Natural Medicines of the Changbai Mountain, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, China.
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Abstract

Objective

Crystals of monosodium urate (MSU) are the cause of gout, a common inflammatory disease. Parthenolide (Par), sesquiterpene lactone, derived from feverfew (Pyrethrum parthenium), possesses potent analgesic, anti-inflammatory, and anticancer properties. However, it remains elusive whether and how Par modulates gout. This research was designed to explore the therapeutic effect and mechanism of Par in acute gout.Methods

Chondrocytes from rat knee joint and mouse peritoneal macrophages (MPMs) were stimulated by lipopolysaccharide (LPS) plus MSU. Combination of yeast extract (YE) with oxygen oxyazine (OXO) was administered to mice to simulate hyperuricemia. MSU crystals were injected into the mice's paws or subcutaneously into the mice's backs to establish acute gouty models.Results

Par blocked the activation of NOD-Like Receptor Pyrin Domains 3 (NLRP3) inflammasome by reducing the expression and release of inflammatory mediators in gouty mice and LPS plus MSU-stimulated MPMs, LPS plus MSU-stimulated chondrocytes as well. Par also promoted phagocytosis abilities of MPMs and chondrocytes to reduce inflammation. In addition, Par dose-dependently reduced the serum levels of uric acid (UA), xanthine oxidase (XOD), creatinine (CRE), and blood urea nitrogen (BUN) and ameliorated renal injury in mice with hyperuricemia.Conclusion

Par ameliorated uric acid metabolism disorders of hyperuricemia, and improved acute gout-like inflammation through the inhibition of NLRP3 inflammasome activation, indicating that Par may be a promising candidate for gout-targeted therapy.

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Cite

BibTeXRIS
BibTeX
@article{cheng2026parthenolide,
  title = {{Parthenolide ameliorated gout-like inflammation by inhibiting activation of NLRP3 inflammasome.}},
  author = {Yonghong Cheng and Yinjing Jiang and Hui Wang and Haoqing Zhu and Yanling Wu and Jixing Nan and Lihua Lian},
  journal = {Chinese herbal medicines},
  year = {2026},
  month = jun,
  doi = {10.1016/j.chmed.2026.06.016},
  url = {https://europepmc.org/article/MED/42948740},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Parthenolide ameliorated gout-like inflammation by inhibiting activation of NLRP3 inflammasome.
AU  - Yonghong Cheng
AU  - Yinjing Jiang
AU  - Hui Wang
AU  - Haoqing Zhu
AU  - Yanling Wu
AU  - Jixing Nan
AU  - Lihua Lian
PY  - 2026
DA  - 2026/06/30
JO  - Chinese herbal medicines
DO  - 10.1016/j.chmed.2026.06.016
UR  - https://europepmc.org/article/MED/42948740
AB  - Objective  Crystals of monosodium urate (MSU) are the cause of gout, a common inflammatory disease. Parthenolide (Par), sesquiterpene lactone, derived from feverfew (Pyrethrum parthenium), possesses potent analgesic, anti-inflammatory, and anticancer properties. However, it remains elusive whether and how Par modulates gout. This research was designed to explore the therapeutic effect and mechanism of Par in acute gout.Methods  Chondrocytes from rat knee joint and mouse peritoneal macrophages (MPMs) were stimulated by lipopolysaccharide (LPS) plus MSU. Combination of yeast extract (YE) with oxygen oxyazine (OXO) was administered to mice to simulate hyperuricemia. MSU crystals were injected into the mice's paws or subcutaneously into the mice's backs to establish acute gouty models.Results  Par blocked the activation of NOD-Like Receptor Pyrin Domains 3 (NLRP3) inflammasome by reducing the expression and release of inflammatory mediators in gouty mice and LPS plus MSU-stimulated MPMs, LPS plus MSU-stimulated chondrocytes as well. Par also promoted phagocytosis abilities of MPMs and chondrocytes to reduce inflammation. In addition, Par dose-dependently reduced the serum levels of uric acid (UA), xanthine oxidase (XOD), creatinine (CRE), and blood urea nitrogen (BUN) and ameliorated renal injury in mice with hyperuricemia.Conclusion  Par ameliorated uric acid metabolism disorders of hyperuricemia, and improved acute gout-like inflammation through the inhibition of NLRP3 inflammasome activation, indicating that Par may be a promising candidate for gout-targeted therapy.
SN  - 1674-6384
SN  - 2589-3610
ER  -