Black tea extract prevents lipopolysaccharide-induced NF-κB signaling and attenuates dextran sulfate sodium-induced experimental colitis

Background: Black tea has been shown to elicit anti-oxidant, anti-carcinogenic, anti-inflammatory and antimutagenic properties. In this study, we investigated the impact of black tea extract (BTE) on lipopolysaccharide (LPS)-induced NF-kappa B signaling in bone marrow derived-macrophages (BMM) and determined the therapeutic efficacy of this extract on colon inflammation. Methods: The effect of BTE on LPS-induced NF-kappa B signaling and pro-inflammatory gene expression was evaluated by RT-PCR, Western blotting, immunofluorescence and electrophoretic mobility shift assay (EMSA). The in vivo efficacy of BTE was assessed in mice with 3% dextran sulfate sodium (DSS)-induced colitis. The severity of colitis was measured by weight loss, colon length and histologic scores. Results: LPS-induced IL-12p40, IL-23p19, IL-6 and IL-1b mRNA expressions were inhibited by BTE. LPS-induced I kappa B alpha phosphorylation/degradation and nuclear translocation of NF-kappa B/p65 were blocked by BTE. BTE treatment blocked LPS-induced DNA-binding activity of NF-kappa B. BTE-fed, DSS-exposed mice showed the less weight loss, longer colon length and lower histologic score compared to control diet-fed, DSS-exposed mice. DSS-induced I kappa B alpha phosphorylation/degradation and phosphorylation of NF-kappa B/p65 were blocked by BTE. An increase of cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP) in DSS-exposed mice was blocked by BTE. Conclusions: These results indicate that BTE attenuates colon inflammation through the blockage of NF-kappa B signaling and apoptosis in DSS-induced experimental colitis model.