The effects of ecabet sodium on nuclear factor-kappa B activation and chemokine gene expression in Helicobacter pylori-infected human gastric epithelial cells.
- Author:
Jung Mogg KIM
1
;
Joo Sung KIM
;
Hyun Chae JUNG
;
Shin Jae KANG
;
Nayang KIM
;
Dong Ho LEE
;
In Sung SONG
Author Information
1. Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Ecabet sodium;
Helicobacter pylori;
Chemokine;
NF-kappa B
- MeSH:
Chemokine CCL2;
Electrophoretic Mobility Shift Assay;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells*;
Gene Expression*;
Genes, Reporter;
Helicobacter pylori;
Helicobacter*;
Humans*;
Interleukin-8;
Luciferases;
NF-kappa B;
RNA, Messenger;
Sodium*
- From:Korean Journal of Medicine
2003;65(2):178-187
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Helicobacter pylori stimulates nuclear factor-kappa B (NF-kappa B) activation and chemokine expression of gastric epithelial cells. Although ecabet sodium (ecabet), a locally acting anti-ulcer drug, is known to have an anti-H. pylori activity, there is little known how ecabet acts anti-inflammatory effects in gastric epithelial cells infected with H. pylori. We investigated the effects of ecabet on chemokine gene expression and NF-kappa B activation of human gastric epithelial cells infected with H. pylori. METHODS: After the infection of Hs746T and MKN-45 gastric epithelial cell lines with cagA+cytotoxin+ H. pylori in the presence of ecabet, mRNA expression of chemokine such as interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) was assessed by quantitative RT-PCR, and chemokine secretion was measured by ELISA. NF-kappa B signals were assayed by electrophoretic mobility shift assay. The activation of NF-kappa B and IL-8 reporter genes was measured by luciferase assay. RESULTS: The treatment of ecabet (5 microgram/mL) decreased the transcription and secretion of chemokine IL-8 and MCP-1 from the gastric epithelial cells infected with H. pylori in a dose-dependent manner. In addition, ecabet inhibited NF-kappa B activation of gastric epithelial cells induced by H. pylori infection. Moreover, the inhibited NF-kappa B signal by ecabet was comprised of heterodimers of p65/p50 predominantly. CONCLUSION: These results suggest that ecabet can inhibit H. pylori-induced IL-8 and MCP-1 gene transcription via suppression of NF-kappa B signal.
