α-Lipoic Acid Inhibits Helicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells
Figure 8
Effect of DPI on expression of β-catenin and c-myc as well as activation of NF-κB and AP-1 in H. pylori-infected AGS cells. The cells were pretreated with DPI for 2 h and cultured in the presence or absence of H. pylori for 24 h (mRNA, protein levels) or 1 h (activation of NF-κB and AP-1). (a) mRNA expression of β-catenin and c-myc was measured by real-time PCR analysis. (b) Protein levels of β-catenin and c-myc were determined by Western blot analysis. Actin served as a loading control. (c), EMSA was performed for DNA binding activities of NF-κB and AP-1. versus corresponding none (the cells cultured in the absence of H. pylori); + versus corresponding H. pylori control (the cells cultured in the presence of H. pylori and treated without DPI).
