Publication | Open Access
Genistein Suppresses LPS-Induced Inflammatory Response through Inhibiting NF-κB following AMP Kinase Activation in RAW 264.7 Macrophages
147
Citations
32
References
2012
Year
Major IsoflavoneImmune RegulationImmunologyRenal InflammationInnate ImmunityOxidative StressInflammationMolecular NutritionCell SignalingMacrophage BiologyInflammatory ResponseChronic InflammationImmune FunctionPharmacologyInflammatory DiseaseRaw 264.7Cell BiologyPhagocyteInflammatory ResponsesCytokineAnti-inflammatoryImmune Cell DevelopmentLps-induced Inflammatory ResponseMedicineAmp Kinase Activation
Genistein, the major isoflavone in soybean, was recently reported to exert beneficial effects in metabolic disorders and inflammatory diseases. In the present study, we investigated the effects and mechanisms of a dietary concentration of genistein on the inflammatory response in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Our results demonstrated that genistein effectively inhibited the LPS-induced overproduction of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6), as well as LPS-induced nuclear factor kappa B (NF-κB) activation. In addition, the data also showed that genistein prevented LPS-induced decrease in adenosine monophosphate-activated protein kinase (AMPK) phosphorylation. These effects were obviously attenuated by an AMPK inhibitor. Taken together, our results suggest that the dietary concentration of genistein is able to attenuate inflammatory responses via inhibition of NF-κB activation following AMPK stimulation. The data provide direct evidence for the potential application of low concentrations of genistein in the prevention and treatment of inflammatory diseases.
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