Synergistic anti-inflammatory effects of quercetin and catechin via inhibiting activation of TLR4-MyD88-mediated NF-κB and MAPK signaling pathways.

Abstract

The synergistic anti-inflammatory effect of quercetin and catechin was investigated using lipopolysaccharide (LPS)-stimulated macrophage RAW 264.7 cells. Results showed that the combined treatment of quercetin with catechin synergistically attenuated LPS-stimulated increase of some proinflammatory molecules, including nitric oxide, tumor necrosis factor α, interleukin-1β, nitric oxide synthase, and cyclooxygenase-2. Moreover, it exhibited significantly (p<0.05) stronger inhibitory effect on nuclear translocation of nuclear factor-κB (NF-κB) by suppressing the phosphorylation of NF-κB p65 and p50 submits and on the phosphorylation of ETS domain-containing protein and c-Jun N-terminal kinase than any of quercetin or catechin alone. Besides, the cotreatment of quercetin with catechin significantly (p<0.05) restored the impaired expression of toll-like receptor 4, myeloid differentiation primary response gene 88, and some downstream effectors (IRAK1, TRAF6, and TAK1). These results suggest that quercetin and catechin possessed synergistic anti-inflammatory effects, which may be attributed to their roles in suppressing the activation of TLR4-MyD88-mediated NF-κB and mitogen-activated protein kinases signaling pathways.