Prunetin inhibits lipopolysaccharide-induced inflammatory cytokine production and MUC5AC expression by inactivating the TLR4/MyD88 pathway in human nasal epithelial cells

Abstract

Allergic rhinitis (AR) is a chronic upper respiratory disorder characterized by inflammation of the nasal mucosa. Prunetin is an O-methylated isoflavone, which has been found to possess anti-inflammatory activity. The aim of the current study was to evaluate the effect of prunetin on inflammatory cytokine and mucus production and its underlying mechanism in nasal epithelial cells. Results showed that treatment with prunetin (10, 30, and 50 μM) inhibited lipopolysaccharide (LPS)-induced expression and secretion of interleukin (IL)-6, IL-8, and mucin 5 AC (MUC5 AC) in RPMI2650 cells, and attenuated the effect of LPS on toll-like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MyD88) expression. TAK-242 (an inhibitor of TLR4) treatment or TLR4 knockdown attenuated LPS-induced expression and secretion of IL-6, IL-8 and MUC5 AC. In conclusion, prunetin inhibited LPS-induced inflammatory cytokine production and MUC5 AC expression and secretion by inactivating the TLR4/MyD88 pathway in human nasal epithelial cells. These results suggested that prunetin might be a useful agent in the treatment of AR.

Keywords: Allergic rhinitis; Inflammatory cytokine; MUC5AC; Prunetin; TLR4/MyD88 pathway.