Modulation of transcription factor NF-κB in Hodgkin's lymphoma cell lines:: Effect of (-)-epicatechin

Transcription factor NF-kappa B plays a central role in tumorogenesis and in different types of cancer, including Hodgkin's lymphoma. Previously, we described that (-)-epicatechin (EC) inhibits PMA-induced NF-kappa B activation in Jurkat T cells. Therefore, we investigated the capacity of EC to inhibit NF-kappa B activation, the underlying mechanisms and the effects of EC on cell viability in Hodgkin's lymphoma cells. EC inhibited NF-kappa B-DNA binding activity in L-428 and KM-H2 cells. This inhibition was not associated with EC antioxidant activity, with changes in p65 phosphorylation or NF-kappa B nuclear translocation. Results suggest that EC acted inhibiting the binding of NF-kappa B to DNA. The combined treatment with EC and an inhibitor of NF-kappa B nuclear translocation (SN-50) caused an additive inhibitory effect on NF-kappa B activation. The partial cell viability decrease, under conditions that EC and SN-50 completely prevented NF-kappa B-DNA binding, indicates that the inhibition of other signaling pathways should be also targeted in the treatment of Hodgkin's lymphoma.