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

• Published in: BMC complementary and alternative medicine Vol. 11; no. 1; p. 91
• Main Authors: Song, Young-A, Park, Young-Lan, Kim, Kyu-Yeol, Chung, Cho-Yun, Lee, Gi-Hoon, Cho, Dae-Ho, Ki, Ho-Seok, Park, Kang-Jin, Cho, Sung-Bum, Lee, Wan-Sik, Kim, Nacksung, Ahn, Bong-Whan, Joo, Young-Eun
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 11.10.2011; BioMed Central; BMC
• Subjects: Animals; Black tea; Camellia sinensis - chemistry; Cells, Cultured; Colitis - chemically induced; Colitis - drug therapy; Colitis - genetics; Colitis - immunology; Colon inflammation; Cytokines - genetics; Cytokines - immunology; Dextran Sulfate - adverse effects; Dextran sulfate sodium; Disease Models, Animal; Down-Regulation - drug effects; Gene Expression - drug effects; Humans; Lipopolysaccharides - immunology; Macrophage; Macrophages - drug effects; Macrophages - immunology; Mice; Mice, Inbred C57BL; NF-kappa B - immunology; NF-κB; Plant Extracts - pharmacology; Signal Transduction - drug effects
• ISSN: 1472-6882; 1472-6882
• DOI: 10.1186/1472-6882-11-91

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. 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 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. 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. These results indicate that BTE attenuates colon inflammation through the blockage of NF-κB signaling and apoptosis in DSS-induced experimental colitis model.