Journal of Environmental Pathology, Toxicology and Oncology

ISSN for PRINT: 0731-8898

For Online Access

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2002, Volume21

Issue 2

124 pages

Issue price - $160.00

Hyeyoung Kim
Department of Pharmacology and Institute ofGastroen-terology, Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, Korea

Joo Weon Lim
Department of Pharmacology and Institute ofGastroen-terology, Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, Korea

Jeong Yeon Seo
Department of Pharmacology and Institute ofGastroen-terology, Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, Korea

Kyung Hwan Kim
Department of Pharmacology and Institute ofGastroen-terology, Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, Korea

Helicobacter pylori (H. pylori) infection might activate nuclear factor-kB (NF-kB), an oxidant-sensitive transcription regulator of inducible expression of inflammatory genes such as cyclooxygenase-2 (COX-2). We studied the role of NF-kB on expression of COX-2 in H. pylori-stimulated gastric cancer cell lines by using antioxidants, glutathione (GSH), and N-acetylcysteine (NAC) as well as an NF-kB inhibitor, pyrrolidine dithiocarbamate (PDTC). Gastric adenocarcinoma cell lines derived from Caucasian (AGS) cells and Korean (SNU-484) cells were used to study the role of NF-kB on COX-2 expression by H. pylori. They were treated with GSH, NAC, or PDTC in the presence of H. pylori. mRNA expression and protein level for COX-2 were determined by Northern blot and RT-PCR analysis as well as Western blot analysis. NF-kB activation was examined by electrophoretic mobility shift assay. As a result, H. pylori induced a time-dependent expression of mRNA and protein for COX-2 via activation of NF-kB, which was inhibited by GSH, NAC, and PDTC in the cells. In conclusion, oxidant-sensitive transcription factor NF-kB may play a novel role in expression of COX-2 by H. pylori stimulation in gastric cancer cells.

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