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

Abstract

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-kappaB (NF-kappaB) 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-kappaB DNA binding activity with capsaicin and immunofluorescence microscopy to examine nuclear staining of p65. We also performed immunoblotting for IkappaB, 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 micromol/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 micromol/L) suppressed H. pylori-induced NF-kappaB activation in gastric epithelial cells at 1 hour post-infection. We also found that the degradation of IkappaB 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 IkappaB-, NF-kappaB-, 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.

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  • Authors+Show Affiliations

    ,

    The Brain Korea 21 Project for Medical Science, Seoul, Korea.

    , , , ,

    Source

    Helicobacter 12:5 2007 Oct pg 510-7

    MeSH

    Anti-Inflammatory Agents, Non-Steroidal
    Capsaicin
    Epithelial Cells
    Gastric Mucosa
    Helicobacter Infections
    Helicobacter pylori
    Humans
    Interleukin-8
    NF-kappa B
    Signal Transduction

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    17760719

    Citation

    Lee, In Ohk, et al. "Anti-inflammatory Effect of Capsaicin in Helicobacter Pylori-infected Gastric Epithelial Cells." Helicobacter, vol. 12, no. 5, 2007, pp. 510-7.
    Lee IO, Lee KH, Pyo JH, et al. Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells. Helicobacter. 2007;12(5):510-7.
    Lee, I. O., Lee, K. H., Pyo, J. H., Kim, J. H., Choi, Y. J., & Lee, Y. C. (2007). Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells. Helicobacter, 12(5), pp. 510-7.
    Lee IO, et al. Anti-inflammatory Effect of Capsaicin in Helicobacter Pylori-infected Gastric Epithelial Cells. Helicobacter. 2007;12(5):510-7. PubMed PMID: 17760719.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Anti-inflammatory effect of capsaicin in Helicobacter pylori-infected gastric epithelial cells. AU - Lee,In Ohk, AU - Lee,Kwang Hyoung, AU - Pyo,Jae Hee, AU - Kim,Jie Hyun, AU - Choi,Yeun Jung, AU - Lee,Yong Chan, PY - 2007/9/1/pubmed PY - 2007/11/2/medline PY - 2007/9/1/entrez SP - 510 EP - 7 JF - Helicobacter JO - Helicobacter VL - 12 IS - 5 N2 - 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-kappaB (NF-kappaB) 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-kappaB DNA binding activity with capsaicin and immunofluorescence microscopy to examine nuclear staining of p65. We also performed immunoblotting for IkappaB, 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 micromol/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 micromol/L) suppressed H. pylori-induced NF-kappaB activation in gastric epithelial cells at 1 hour post-infection. We also found that the degradation of IkappaB 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 IkappaB-, NF-kappaB-, 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. SN - 1083-4389 UR - https://www.unboundmedicine.com/medline/citation/17760719/Anti_inflammatory_effect_of_capsaicin_in_Helicobacter_pylori_infected_gastric_epithelial_cells_ L2 - https://doi.org/10.1111/j.1523-5378.2007.00521.x DB - PRIME DP - Unbound Medicine ER -