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Anti-inflammatory Effect of Capsaicin in Helicobacter pylori-Infected Gastric Epithelial Cells

 In Ohk Lee  ;  Kwang Hyoung Lee  ;  Yong Chan Lee  ;  Yeun Jung Choi  ;  Jie Hyun Kim  ;  Jae Hee Pyo 
 HELICOBACTER, Vol.12(5) : 510-517, 2007 
Journal Title
Issue Date
Anti-Inflammatory Agents, Non-Steroidal/pharmacology* ; Capsaicin/pharmacology* ; Epithelial Cells/drug effects ; Epithelial Cells/immunology* ; Epithelial Cells/microbiology ; Gastric Mucosa/cytology ; Gastric Mucosa/drug effects ; Gastric Mucosa/immunology* ; Gastric Mucosa/microbiology ; Helicobacter Infections/microbiology ; Helicobacter pylori/drug effects ; Helicobacter pylori/pathogenicity* ; Humans ; Interleukin-8/antagonists & inhibitors* ; Interleukin-8/biosynthesis ; NF-kappa B/metabolism ; Signal Transduction/drug effects
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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1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Jie-Hyun(김지현) ORCID logo https://orcid.org/0000-0002-9198-3326
Lee, Yong Chan(이용찬) ORCID logo https://orcid.org/0000-0001-8800-6906
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