Publication | Closed Access
Synergistic anti‐inflammatory effects of quercetin and catechin via inhibiting activation of TLR4–MyD88‐mediated NF‐κB and MAPK signaling pathways
120
Citations
23
References
2019
Year
Inflammatory Lung DiseaseLung InflammationNitric OxideImmunologyImmune RegulationRenal InflammationInnate ImmunityImmune DysregulationOxidative StressInflammationMolecular PharmacologyTlr4–myd88‐mediated Nf‐κbTumor ImmunityCell SignalingMolecular SignalingMedicineChronic InflammationImmune FunctionPharmacologySynergistic Anti‐inflammatory EffectsInflammatory DiseaseSynergistic Anti-inflammatory EffectCytokineAnti-inflammatoryMacrophage Raw 264.7Mapk Signaling Pathways
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.
| Year | Citations | |
|---|---|---|
Page 1
Page 1