Astaxanthin inhibits mitochondrial dysfunction and IL-8 expression in Helicobacter pylori-infected gastric epithelial cells Suhnhyung Kim, Joo Weon Lim, Hyeyoung Kim Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 03722, Korea Backgrounds and purpose: Helicobacter pylori (H. pylori) infection is a risk factor for gastritis and gastric cancer. H. pylori induces NADPH oxidase-mediated reactive oxygen species (ROS) production, which leads to inflammatory cytokine production. In several cell lines, mitochondrial ROS act as signaling molecule to trigger inflammatory cytokine production. Increased oxidative stress and mitochondrial dysfunction is associated with gastritis.Astaxanthin (AST) is an antioxidant known to protect cells against ROS production in vivo and in vitro. The present study was undertaken to determine whether H. pylori induces mitochondrial dysfunction and ROS-mediated IL-8 expression, and whether AST inhibits mitochondrial dysfunction and IL-8 expression in gastric epithelial cells infected with H. pylori. Methods: Human gastric epithelial AGS cells were infected with H. pylori (NCTC11637) at bacterium/cell ratio of 50:1. Intracellular and mitochondrial ROS were measured using DCF-DA and MitoSox fluorescence, respectively. Mitochondrial membrane potential (MMP) and ATP level was measured by flow cytometric analysis and kit assay, respectively. IL-8 mRNA expression was determined using real-time PCR analysis. Results: H. pylori induced IL-8 expression as well as production of intracellular and mitochondrial ROS in AGS cells. H. pylori decreased MMP and intracellular ATP level in AGS cells, indicating that H. pylori cause's mitochondrial dysfunction. Apocynin, NADPH oxidase inhibitor, inhibited H. pylori-induced mitochondrial ROS production and IL-8 expression. The results demonstrate that NADPH oxidase activation mediates H. pylori-induced mitochondrial ROS production and inflammatory signaling. AST inhibited H. pylori-induced ROS production, mitochondrial dysfunction, and IL-8 expression in the cells. These results suggest that AST inhibits H. pylori-induced IL-8 expression through suppressing mitochondrial dysfunction and ROS production in gastric epithelial cells. Conclusions: AST may inhibit gastric inflammation associated with H. pylori infection by suppressing ROS-mediated IL-8 expression and preventing mitochondrial dysfunction in gastric epithelial cells.
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