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   <subfield code="a">10.1007/s00011-010-0297-y</subfield>
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   <subfield code="a">Diphenyleneiodonium inhibits the activation of mitogen-activated protein kinases and the expression of monocyte chemoattractant protein-1 in Helicobacter pylori -infected gastric epithelial AGS cells</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Soon Cho, Joo Lim, Kyung Kim, Hyeyoung Kim]</subfield>
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   <subfield code="a">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.</subfield>
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   <subfield code="u">Department of Pharmacology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, 120-752, Seoul, Korea</subfield>
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   <subfield code="u">Department of Food and Nutrition, Brain Korea 21 Project, College of Human Ecology, Yonsei University, 120-749, Seoul, Korea</subfield>
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   <subfield code="u">Department of Pharmacology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, 120-752, Seoul, Korea</subfield>
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   <subfield code="t">Inflammation Research</subfield>
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