α-Lipoic Acid Inhibits Helicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells
Figure 2
ROS levels, NADPH oxidase activity, and mRNA and protein levels of β-catenin and c-myc in AGS cells infected with H. pylori. (a, b, d, f) The cells were cultured in the presence or absence of H. pylori (at bacterium/cell ratio of 10, 20, 50 : 1) for 24 h. (c, e) AGS cells were cultured in the presence or absence of H. pylori (bacterium/cell ratio of 50 : 1) for the indicated time period. (a) ROS levels were determined by DCF fluorescence after 30 min of H. pylori infection. The levels of ROS trapped in the cells and cultured in the absence of H. pylori (none) are considered as 100%. (b) NADPH oxidase activity was determined by lucigenin assay using membrane extracts of the cells. NADPH oxidase activity was also monitored by addition of cytosolic extracts to the reaction mixture as a negative control. (c–f) mRNA and protein expression were determined by real-time PCR and Western blot analysis, respectively. Actin served as a loading control. versus 0 h or none (the cells cultured in the absence of H. pylori).
