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- Title
The phenyl-thiophenyl propenone RK-I-123 reduces the levels of reactive oxygen species and suppresses the activation of NF-κB and AP-1 and IL-8 expression in Helicobacter pylori-infected gastric epithelial AGS cells.
- Authors
Jang, Sung; Cho, Soonok; Lee, Eung-Seok; Kim, Jung; Kim, Hyeyoung
- Abstract
Objective: To investigate whether the phenyl-thiophenyl propenone RK-I-123 suppresses interleukin-8 (IL-8) expression and activation of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activator protein-1 [AP-1]) by reducing reactive oxygen species (ROS) levels in Helicobacter pylori-infected gastric epithelial cells. Material: Helicobacter pylori in Korean isolates, human gastric epithelial AGS cells. Treatment: AGS cells pretreated with or without RK-I-123 were cultured in the presence of H. pylori at a bacterium/cell ratio of 300:1. Methods: Reactive oxygen species and IL-8 levels were determined by dichlorofluorescein fluorescence and enzyme-linked immunosorbent assay. The IL-8 mRNA expression was analyzed by the real-time reverse transcription-polymerase chain reaction (RT-PCR). The MAPK and IκBα levels were determined by western blotting. The activation of NF-κB and AP-1 was determined by the electrophoretic mobility shift assay. Results: Helicobacter pylori induced an increase in ROS and IL-8 expression and activation of MAPKs and transcription factors (NF-κB and AP-1) together with the degradation of IκBα in AGS cells, all of which were inhibited by RK-I-123. Conclusions: The RK-I-123 suppressed the H. pylori-induced IL-8 expression and activation of MAPKs, NF-κB, and AP-1 by reducing ROS levels in AGS cells. The RK-I-123 may be a potential candidate for the treatment of H. pylori-induced gastric inflammation.
- Subjects
REACTIVE oxygen species; NF-kappa B; AP-1 transcription factor; INTERLEUKIN-8; HELICOBACTER pylori infections; EPITHELIAL cells; GENE expression; PHENYL compounds
- Publication
Inflammation Research, 2013, Vol 62, Issue 7, p689
- ISSN
1023-3830
- Publication type
Article
- DOI
10.1007/s00011-013-0621-4