BMC Complementary and Alternative Medicine | |
Black tea extract prevents lipopolysaccharide-induced NF-κB signaling and attenuates dextran sulfate sodium-induced experimental colitis | |
Young-Eun Joo3  Bong-Whan Ahn2  Nacksung Kim1  Wan-Sik Lee3  Sung-Bum Cho3  Kang-Jin Park3  Ho-Seok Ki3  Dae-Ho Cho3  Gi-Hoon Lee3  Cho-Yun Chung3  Kyu-Yeol Kim3  Young-Lan Park3  Young-A Song3  | |
[1] Department of Pharmacology, Chonnam National University Medical School, Gwangju, Korea;Department of Biochemistry, Chonnam National University Medical School, Gwangju, Korea;Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea | |
关键词: Colon inflammation; Dextran sulfate sodium; Macrophage; NF-κB; Black tea; | |
Others : 1232957 DOI : 10.1186/1472-6882-11-91 |
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received in 2011-05-09, accepted in 2011-10-11, 发布年份 2011 | |
【 摘 要 】
Background
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.
Methods
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.
Results
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.
Conclusions
These 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】
2011 Song et al; licensee BioMed Central Ltd.
【 预 览 】
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