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

BMC Complementary and Alternative Medicine

Research Article

Bong-Whan Ahn¹  Kyu-Yeol Kim²  Gi-Hoon Lee²  Young-Lan Park²  Kang-Jin Park²  Wan-Sik Lee²  Cho-Yun Chung²  Ho-Seok Ki²  Dae-Ho Cho²  Sung-Bum Cho²  Young-Eun Joo²  Young-A Song²  Nacksung Kim³ 

[1] Department of Biochemistry, Chonnam National University Medical School, Gwangju, South Korea;Department of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea;Department of Pharmacology, Chonnam National University Medical School, Gwangju, South Korea;

关键词: Black tea;    NF-κB;    Macrophage;    Dextran sulfate sodium;    Colon inflammation;   

DOI  :  10.1186/1472-6882-11-91

 received in 2011-05-09, accepted in 2011-10-11,  发布年份 2011

来源: Springer

【 摘 要 】

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

【 授权许可】

Unknown   
© Song et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.