Protective effects of di-caffeoylquinic acids from Artemisia selengensis Turcz leaves against monosodium urate-induced inflammation via the modulation of NLRP3 inflammasome and Nrf2 signaling pathway in THP-1 macrophages

Artemisia selengensis Turcz (AST) as a common vegetable is rich in di-caffeoylquinic acids (di-CQAs) and has been reported to possess multiple health benefits. However, whether di-CQAs from AST leaf extracts (ASTE) could alleviate gout inflammation is still unknown. Herein, this study explored the inhibitory mechanism of ASTE on gout inflammation in THP-1 macrophages. Results suggested that ASTE suppressed the secretion and mRNA levels of inflammatory cytokines including interleukin-18, interleukin-1β, interleukin-6, and tumor necrosis factor-α. Pretreatment with ASTE inhibited lipopolysaccharide-induced of IκBα degradation, p65 phosphorylation and up-regulation of Nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome proteins. Moreover, ASTE inhibited monosodium urate-induced the up-regulation of active Caspase-1 and interleukin-1β, promoted nuclear factor E2-related factor2 (Nrf2) to translocate into the nucleus, reducing the generation of MSU-induced Reactive Oxygen Species. These results suggested that ASTE alleviated gout inflammation via inhibiting NLRP3 inflammasome activation and activating Nrf2 signaling pathway. PRACTICAL APPLICATIONS: Artemisia selengensis Turcz (AST) as a common vegetable in China belongs to genus Artemisia, which are rich in di-caffeoylquinic acids. This study aimed to investigate the effect of ASTE on alleviating gout inflammation and whether NLRP3 inflammasome and Nrf2 signaling pathways are involved in the protection of ASTE against gout inflammation. Our findings are significant for developing di-CQAs from AST by-products as an effective functional food for preventing gout.