4.6 Article

Taxifolin blocks monosodium urate crystal-induced gouty inflammation by regulating phagocytosis and autophagy

Journal

INFLAMMOPHARMACOLOGY
Volume 30, Issue 4, Pages 1335-1349

Publisher

SPRINGER BASEL AG
DOI: 10.1007/s10787-022-01014-x

Keywords

Acute gout; Autophagy; IL-1 beta; Inflammation; Taxifolin

Funding

  1. National Natural Science Foundation of China [82074095, 81960677]
  2. National Key Research and Development Program of China [2019YFC1712500]

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This study demonstrates that Taxifolin can alleviate inflammation in MSU-induced acute gout by enhancing autophagy and phagocytic capacity of macrophages.
Gout is a chronic disease caused by monosodium urate (MSU) crystal deposition in the joints and surrounding tissues. We examined the effects of Taxifolin, a natural flavonoid mainly existing in vegetables and fruits, on MSU-induced gout. Pretreatment with Taxifolin significantly reduced IL-1 beta, Caspase-1 and HMGB1 levels, upregulation of autophagy-related protein, LC3, as well as improved phagocytosis of macrophages. This study indicated that Taxifolin-attenuated inflammatory response in MSU-induced acute gout model by decreasing pro-inflammatory cytokine production and promoting the autophagy and phagocytic capacity of macrophages. Dietary supplementation with Taxifolin induces the autophagy and attenuated inflammatory response, which in consequence modulates acute gout. A preventive strategy combining dietary interventions with Taxifolin may offer a potential therapeutic alternative to pharmacological treatment to reduce inflammatory response to gout.

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