Abstract
Quercetin (3,3′,4′,5,6-pentahydroxyflavone) is a well-known antioxidant and a flavonol found in many fruits, leaves, and vegetables. Quercetin also has known anti-inflammatory effects on lipopolysaccharide-induced macrophages. However, the effects of quercetin on virus-induced macrophages have not been fully reported. In this study, the anti-inflammatory effect of quercetin on double-stranded RNA (dsRNA)-induced macrophages was examined. Quercetin at concentrations up to 50 μM significantly inhibited the production of NO, IL-6, MCP-1, IP-10, RANTES, GM-CSF, G-CSF, TNF-α, LIF, LIX, and VEGF as well as calcium release in dsRNA (50 µg/mL of polyinosinic-polycytidylic acid)-induced RAW 264.7 mouse macrophages (p < 0.05). Quercetin at concentrations up to 50 μM also significantly inhibited mRNA expression of signal transducer and activated transcription 1 (STAT1) and STAT3 in dsRNA-induced RAW 264.7 cells (p < 0.05). In conclusion, quercetin had alleviating effects on viral inflammation based on inhibition of NO, cytokines, chemokines, and growth factors in dsRNA-induced macrophages via the calcium-STAT pathway.
Highlights
Immunity is essential for life and innate immunity provides the first line of response to invading pathogens [1]
264.7 mouse macrophages were incubated with poly(I:C) and/or quercetin for 24 h, and 100 μL of mouse macrophages incubated with100 poly(I:C)
The present study shows that quercetin may alleviate poly(I:C)-induced inflammation by decreasing levels of inflammatory mediators, such as nitric oxide (NO), cytokines, chemokines, and growth factors, in RAW 264.7 mouse macrophages; quercetin is a candidate for modulating virus-hyperinflammation such as a cytokine storm
Summary
Immunity is essential for life and innate immunity provides the first line of response to invading pathogens [1]. Viruses can induce tissue necrosis and inflammation and viral infections activate the immune response, trigger inflammatory diseases, and promote cancer growth [6]. DsRNA, which is recognized by Toll-like receptor-3, induces the production of inflammatory mediators, such as NO, interleukin (IL)-6, and tumor necrosis factor (TNF)-α, in macrophages; polyinosinic-polycytidylic acid (poly(I:C)). The effects of quercetin on poly(I:C)-induced macrophages have not quercetin poly(I:C)‐induced macrophages have not been fully reported. Quercetin at concentrations up to 50 μM significantly inhibited the production production of various factors, as well as calcium release and mRNA expression of signal transducer of various factors, as well as calcium release and mRNA expression of signal transducer and activated and activated transcription 1 (STAT1) and STAT3 in poly(I:C)‐induced RAW 264.7 mouse transcription 1 (STAT1) and STAT3 in poly(I:C)-induced RAW 264.7 mouse macrophages
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