Inhibitory Effect of Capsaicin on Interleukin-8 Production by Helicobacter pylori-Infected MKN-45 Cells

  • Lee, Kwang-Hyoung (Division of Animal Life Science and Animal Resource Research Center, Konkuk University) ;
  • Lee, Yong-Chan (Department of Intestinal Gastroenterology, College of Medicine, Yonsei Univeristy) ;
  • Kim, Tae-Il (Department of Intestinal Gastroenterology, College of Medicine, Yonsei Univeristy) ;
  • Noh, Sung-Hoon (Department of Surgery, College of Medicine, Yonsei University) ;
  • Kim, Ji-Yeon (Department of Animal Science, Woosong Information College) ;
  • Paik, Hyun-Dong (Division of Animal Life Science and Animal Resource Research Center, Konkuk University) ;
  • Kim, Chang-Han (Division of Animal Life Science and Animal Resource Research Center, Konkuk University)
  • Published : 2006.07.01

Abstract

Capsaicin is the active ingredient in chili pepper and has an inhibitory effect on Helicobacter pylori growth and $NF-{\kappa}B$ activation. The present study examined the effect of capsaicin on interleukin (IL)-8 production by H. pylori ATCC 43504-infected MKN-45 cells, a gastric epithelial cell line. The viability of the MKN-45 cells treated with capsaicin at 0, 50, 100, 250, and $500\;{\mu}M$ was 99, 98, 99, 99, and 85%, respectively. A capsaicin concentration as low as $50\;{\mu}M$ significantly inhibited the IL-8 production induced by H. pylori ATCC 43504 infection (43.2% of control) during 24 h of incubation. However, low concentrations of capsaicin $(50\;and\;100{\mu}M)$ did not significantly inhibit the IL-8 production by $TNF-{\alpha}-$ or PMA-treated MKN-45 cells. Therefore, the overall inhibitory effect of capsaicin on H. pylori ATCC 43504 was the sum of H. pylori ATCC 43504 growth inhibition, host cell survival, and $NF-{\kappa}B$ signal cascade inhibition.

Keywords

References

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