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대한Helicobacter 연구학회지 2003;3(1):1-12.
Published online June 30, 2003.
Effect of Inhibition of Extracellular Signal-Regulated Kinase 1/2 on NF-kB Activation and Apoptosis in Helicobacter pylori-Infected AGS Cells
Helicobacter pylori에 감염된 AGS 세포주에서 Extracellular Signal-Regulated Kinase 1/2 경로의 억제가 NF-kB 활성화와 아포토시스에 미치는 영향
최일주*·김주성·김정목·정현채·송인성
*국립암센터 위암센터, 한양대학교 의과대학 미생물학교실, 서울대학교 의과대학 내과학교실 및 간연구소
Abstract
Background/Aims: Helicobacter pylori induces activation of MAP kinases. However, its effect on H. pylori-induced apoptosis and NF-kB activation has not been fully evaluated. We examined whether H. pylori-induced MAP kinase activation affects NF-kB activation and apoptosis. Methods: AGS cells were co-cultured with H. pylori with or without pretreatment of MAP kinase inhibitors. NF-kB activation was assessed by western blot analysis for IkB, immunocytochemical staining, and electrophoretic mobility shift assay. MAP kinase activation was determined by western blot analysis for phosphorylated ERK1/2 or p38. The mRNA expressions of IL-8 and bcl-2 related genes were measured by RT-PCR. Apoptosis was evaluated by flowcytometry and ELISA methods. Results: Infection with cagA H. pylori strains induced activation of ERK1/2 and p38 MAP kinases, NF-kB activation and apoptosis. Pretreatment with PD98059 to inhibit ERK1/2 activation decreased NF-kB activation and increased apoptosis. The increased apoptosis was accompanied by a decrease of the antiapoptotic bcl-2 gene expression. Those results were more prominent in the cagA strains. Inhibition of p38 MAP kinase decreased H. pylori-induced apoptosis, but resulted in little alteration of bcl-2 related gene expression. Conclusions: ERK1/2 activation by H. pylori cause inflammatory response by NF-kB activation and play a protective role against apoptosis through maintaining the bcl-2 gene expression. (Korean J Helicobacter Res Prac 2003;3:1-12)
Key Words: Helicobacter pylori, Extracellular signal-regulated kinase 1/2, NF-kB, Apoptosis, bcl-2
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