Objective: To investigate whether NADPH oxidase induces MCP-1 expression and the activation of mitogen-activated protein kinases (MAPKs) in H. pylori-infected gastric epithelial cells. Material: H. pylori in Korean isolates, human gastric epithelial AGS cells Treatment: AGS cells pretreated with or without an NADPH oxidase inhibitor diphenyleneiodonium (DPI) are cultured in the presence of H. pylori at a bacterium/cell ratio of 300:1. Methods: Reactive oxygen species (ROS) and MCP-1 were determined by confocal microscopy and enzyme-linked immonosorbent assay. NADPH oxidase activity was measured by lucigenin assay. mRNA expression of MCP-1 was analyzed by reverse transcription-polymerase chain reaction. Levels of MAPKs were assessed by Western blot analysis. Results: H. pylori induced increase in ROS, NADPH oxidase activity, MCP-1 expression, and the activation of MAPKs including extracellular signal-regulated kinases, p38, and jun N-terminal kinases in AGS cells, which was inhibited by DPI. Conclusion: Inhibiting NADPH oxidase by DPI suppresses H. pylori-induced activation of MAPKs and MCP-1 expression in AGS cells.
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Acknowledgments This study was supported by a grant (Joint Research Project under the Korea-Japan Basic Scientific Cooperation Program) from NRF (F01-2009-000-10101-0) and the grants from Basic Science Research Program through NRF funded by the Ministry of Education, Science and Technology (2010-0001669, 2010-0002916). H. Kim is grateful to the Brain Korea 21 Project, college of Human Ecology, Yonsei University.
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