Taxifolin blocks monosodium urate crystal-induced gouty inflammation by regulating phagocytosis and autophagy.
Mei-Hua PiaoHui WangYin-Jing JiangYan-Ling WuJi-Xing NanLi-Hua LianPublished in: Inflammopharmacology (2022)
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-1β, 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.
Keyphrases
- cell death
- inflammatory response
- uric acid
- oxidative stress
- endoplasmic reticulum stress
- diabetic rats
- signaling pathway
- high glucose
- drug induced
- induced apoptosis
- lipopolysaccharide induced
- lps induced
- metabolic syndrome
- gene expression
- liver failure
- physical activity
- poor prognosis
- cell proliferation
- intensive care unit
- risk assessment
- mass spectrometry
- extracorporeal membrane oxygenation
- climate change
- acute respiratory distress syndrome
- solid state
- liquid chromatography