RESUMO
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.