Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Quercetin Exerts Anti-Inflammatory Effects via Meanwhile Suppressing TLR2 Gene Expression and STAT3 Protein Phosphorylation in Activated Inflammatory Macrophages

Version 1 : Received: 19 November 2019 / Approved: 20 November 2019 / Online: 20 November 2019 (16:04:42 CET)

A peer-reviewed article of this Preprint also exists.

Journal reference: Journal of Exploratory Research in Pharmacology 2020, 1-11
DOI: 10.14218/JERP.2020.00006

Abstract

Our previous studies demonstrated that quercetin (Q) could be ingested and metabolized by macrophages and exerted prophylactic immuno-stimulatory activity and therapeutic anti-inflammatory effects on lipopolysaccharide (LPS)-treated macrophages ex vivo. To further clarify its possible anti-inflammatory mechanism, Q was selected to treat mouse peritoneal macrophages that obtained from female BALB/c mice exposed to LPS i.p. for 12 h. Relative gene expression of pro-/anti-inflammatory (TNF-α/IL-10) cytokines and components of inflammation-related intracellular signaling pathways (TLR2, TLR4, NF-κB, JAK2 and STAT3) was analyzed using two-step reverse transcription (RT) and real-time quantitative polymerase chain reaction (qPCR). STAT3 protein phosphorylation was determined using an in-cell ELISA method. As a result, Q and its metabolite quercetin-3-O-β-D-glucuronide (Q3G) decreased TNF-α gene expression amounts and ratios of pro-/anti-inflammatory (TNF-α/IL-10) cytokine gene expressions, but increased IL-10 gene expression amounts in activated inflammatory macrophages, supporting a substantial anti-inflammatory potential of Q and Q3G treatments. However, Q3G had lower effects than those of Q. Importantly, Q inhibited TLR2 gene expression and phosphorylation of STAT3 protein in the inflamed cells. Our results are the first report to suggest that Q inhibits LPS-induced inflammation ex vivo through suppressing TLR2 gene expression and STAT3 protein phosphorylation in activated inflammatory macrophages. Q has potential to further apply for treating inflammation-associated diseases.

Subject Areas

activated inflammatory macrophages; quercetin; pro-/anti-inflammatory cytokine genes; STAT3 protein phosphorylation; TLR2

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