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

• Main Authors: Cho Sung-Bum, Park Kang-Jin, Ki Ho-Seok, Cho Dae-Ho, Lee Gi-Hoon, Chung Cho-Yun, Kim Kyu-Yeol, Park Young-Lan, Song Young-A, Lee Wan-Sik, Kim Nacksung, Ahn Bong-Whan, Joo Young-Eun
• Format: Article
• Language: English
• Published: BMC 2011-10-01
• Series: BMC Complementary and Alternative Medicine
• Subjects: Black tea; NF-κB; Macrophage; Dextran sulfate sodium; Colon inflammation
• Online Access: http://www.biomedcentral.com/1472-6882/11/91

<p>Abstract</p> <p>Background</p> <p>Black tea has been shown to elicit anti-oxidant, anti-carcinogenic, anti-inflammatory and anti-mutagenic properties. In this study, we investigated the impact of black tea extract (BTE) on lipopolysaccharide (LPS)-induced NF-κB signaling in bone marrow derived-macrophages (BMM) and determined the therapeutic efficacy of this extract on colon inflammation.</p> <p>Methods</p> <p>The effect of BTE on LPS-induced NF-κB signaling and pro-inflammatory gene expression was evaluated by RT-PCR, Western blotting, immunofluorescence and electrophoretic mobility shift assay (EMSA). The <it>in vivo </it>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.</p> <p>Results</p> <p>LPS-induced IL-12p40, IL-23p19, IL-6 and IL-1β mRNA expressions were inhibited by BTE. LPS-induced IκBα phosphorylation/degradation and nuclear translocation of NF-κB/p65 were blocked by BTE. BTE treatment blocked LPS-induced DNA-binding activity of NF-κB. 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 IκBα phosphorylation/degradation and phosphorylation of NF-κB/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.</p> <p>Conclusions</p> <p>These results indicate that BTE attenuates colon inflammation through the blockage of NF-κB signaling and apoptosis in DSS-induced experimental colitis model.</p>