Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells

被引:71
作者
Lee, In Ohk
Lee, Kwang Hyoung
Pyo, Jae Hee
Kim, Jie Hyun
Choi, Yeun Jung
Lee, Yong Chan
机构
[1] Yonsei Univ, Sch Med, Dept Internal Med, Seoul 120749, South Korea
[2] Yonsei Univ, Coll Med, Braub Korea 21 Project Med Sci, Seoul 120749, South Korea
[3] Yonsei Univ, Coll Med, Dept Internal Med, Div Gastroenterol, Seoul 120749, South Korea
[4] CHA Biomed, R&D Ctr, Gangnam, South Korea
关键词
capsaicin; H.pylori; IL-8; NF-kappa B;
D O I
10.1111/j.1523-5378.2007.00521.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background and aim: Capsaicin, the main pungent ingredient of hot red and chilli pepper, has been considered as not only a cytoprotective but also a detrimental agent to the gastric mucosa. However, the effect and mechanism of capsaicin that modulate the induction of pro-inflammatory cytokine in Helicobacter pylori-infected epithelial cells have not been investigated previously. Herein, we demonstrated that capsaicin inhibited the release of pro-inflammatory cytokine, interleukin-8 (IL-8) by H. pylori-infected gastric epithelial cells through nuclear factor-kappa B (NF-kappa B) signal pathway. Materials and methods: AGS or MKN45 cells as gastric epithelial cells and Vac A+, CagA+ wild-type H. pylori strain ATCC 49503 were used. Gastric epithelial cells were pre-treated with various concentrations of capsaicin and infected with H. pylori for different periods of time to determine IL-8 concentrations in culture supernatant by an ELISA assay. We measured IL-8 mRNA transcripts in H. pylori-infected gastric epithelial cells co-treated with capsaicin by reverse transcriptase-polymerase chain reaction analysis. We performed electrophoretic mobility shift assay to examine the NF-kappa B DNA binding activity with capsaicin and immunofluorescence microscopy to examine nuclear staining of p65. We also performed immunoblotting for I kappa B, IKK activity with capsaicin. Results: Capsaicin inhibits H. pylori-induced IL-8 production by gastric epithelial cells in dose- and time-dependent manner. Capsaicin as low as 100 mu mol/L significantly inhibited IL-8 production in H. pylori-infected MKN45 cells (43.2% of control) at 24 hours incubation, whereas inhibited IL-8 production in H. pylori-infected AGS cells (70% of control). We confirmed that capsaicin inhibited IL-8 mRNA expression after infection of gastric epithelial cells with H. pylori for 6 hours. The addition of capsaicin (100 mu mol/L) suppressed H. pylori-induced NF-kappa B activation in gastric epithelial cells at 1 hour post-infection. We also found that the degradation of I kappa B and IKK activation were inhibited by capsaicin. Conclusions: Nontoxic dose of capsaicin inhibited H. pylori-induced IL-8 production by gastric epithelial cells through the modulation of I kappa B-, NF-kappa B-, and IL-8 pathways. We conclude that capsaicin can be proposed as a potential anti-inflammatory drug by inhibition of the production of IL-8 in H. pylori-infected gastric epithelium.
引用
收藏
页码:510 / 517
页数:8
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