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

BMC Complementary and Alternative Medicine

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

 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.

【 图 表 】

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