Inhibitory effects of 7-carboxymethyloxy-3',4',5-trimethoxyflavone (DA-6034) on Helicobacter pylori-induced NF-kappa B activation and iNOS expression in AGS cells

• Published in: Annals of the New York Academy of Sciences Vol. 1095; pp. 527 - 535
• Main Authors: Lee, Jeong-Sang, Kim, Hyun-Soo, Hahm, Ki-Baik, Sohn, Mi-Won, Yoo, Moohi, Johnson, Jeffrey A, Surh, Young-Joon
• Format: Journal Article
• Language: English
• Published: United States 01.01.2007
• Subjects: Anti-Inflammatory Agents, Non-Steroidal - pharmacology; Cell Line, Tumor; Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors; Extracellular Signal-Regulated MAP Kinases - metabolism; Flavonoids - pharmacology; Gastric Mucosa - drug effects; Gastric Mucosa - enzymology; Gastric Mucosa - microbiology; Gastric Mucosa - pathology; Helicobacter pylori - physiology; Humans; NF-kappa B - antagonists & inhibitors; NF-kappa B - metabolism; Nitric Oxide Synthase Type II - antagonists & inhibitors; Nitric Oxide Synthase Type II - biosynthesis; Nitric Oxide Synthase Type II - genetics
• ISSN: 0077-8923

The Helicobacter pylori were identified by Marshall and Warren in 1984. H. pylori survive in the forbidding harsh acid environment of the stomach and duodenum by hiding in the mucus layer and neutralizing gastric acid in its local surrounding environment. Multiple lines of evidence suggest that H. pylori infection is one of the primary causes of gastritis and peptic ulcer, which are provoked by oxidative stress and inflammation. More than 50% of the world's population is infected by this bacterium. The H. pylori-induced inflammation has been implicated in the pathogenesis and progression of gastric cancer. DA-6034 (7-carboxymethyloxy-3',4',5-trimethoxy flavone) is a synthetic flavonoid known to possess anti-inflammatory activity. It has been reported that oral administration of DA-6034 suppresses the inflammatory bowel disease (IBD) in animal models. In this article, we attempted to examine the effect of DA-6034 on H. pylori-induced inflammation in human gastric cancer (AGS) cells by targeting NF-kappaB and extracellular signal-regulated kinase (ERK), a representative MAPK.