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Regulatory effects of emodin on NF-κB activation and inflammatory cytokine expression in RAW 264.7 macrophages
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2005
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Regulatory EffectsImmune RegulationImmunologyInnate ImmunityOxidative StressInflammationInflammatory MarkerCell SignalingAnthraquinones ComponentInflammatory CytokinesAllergyAutoimmune DiseaseChronic InflammationAutoimmunityImmune FunctionInflammatory DiseaseRaw 264.7Cell BiologyPhagocyteCytokineAnti-inflammatorySignal TransductionInflammation BiologyNf-κb ActivationMedicine
Emodin, an anthraquinones component of Rheum palmatun, has been used for anti-inflammatory purposes. However, its underlying molecular effect(s) on target cells remain to be well clarified. Thus, our current study was aimed at investigating the regulatory mechanism of emodin on liposaccharide-induced inflammatory responses in RAW 264.7 macrophages by RT-PCR, Western blot analysis, immunocytochemical staining and immunofluorescence analysis. It was found that a treatment of 20 microg/ml emodin inhibited the expression of a panel of inflammatory-associated genes, including TNFalpha, iNOS, IL-10, cytosolic IkappaBalpha, IKK-alpha and IKK-gamma, to different extents as well as the nuclear translocation of NF-kappaB (nuclear factor-kappaB). The promoting effect of emodin on the production and translocation of p105 (the precursor of NF-kappaB p50) was time-dependent and reached a maximum at 5 h. Our data suggest that emodin plays its anti-inflammatory roles by regulating inflammatory cytokines, specifically by suppressing NF-kappaB activation.