Inhibition of Helicobacter pylori CagA-Induced Pathogenesis by Methylantcinate B from Antrodia camphorata
Figure 1
Methylantcinate B (MAB) influences H. pylori (Hp) CagA expression, translocation, and phosphorylation. AGS cells were treated with indicated concentrations of MAB prior infection by Hp at MOI 100 for 6 h. (a) The samples were immunoprecipitated for CagA and subjected to western blot analysis. Actin was represented as an internal control for equal loading. The levels of CagA translocation (b) and CagA phosphorylation (c) were determined by densitometric analysis. (d) The proportions of elongated cells were evaluated after cells cocultured with Hp and MAB for 6 h. (e) The hummingbird phenotype cells were determined. Results were shown as mean values ± standard deviations from 3 independent experiments. * and ** were considered as statistically significant. Arrows in (d) represented elongated hummingbird phenotypes of AGS cells. Scale bar, 10 μm.
