Fig. 3. CBS inhibits the growth of H. pylori by attacking the oxidative stress defence and the pH-buffering systems. (A) Growth of H. pylori under oxidative stress from various donors without (control) and with CBS treatment. Under the stress of various ROS donors, the growth of Bi-treated bacterium was significantly lower than the control groups, implying its reduced ability for defence against these oxidative stress donors. The activities of three enzymes, AhpC, arginase and KatA, were inhibited by Bi (B–D). (E) Intracellular pH of H. pylori indicated by the fluorescent probe LysoSensor™. Under acidic conditions (pH = 4.0), Bi-treated bacteria exhibited acidic intracellular pH, while the untreated bacteria could keep the intracellular pH as neutral. Under neutral conditions (pH = 7.0), Bi treatment did not induce obvious changes in the bacterial intracellular pH. The growth of Bi-treated bacterium was significantly inhibited under acidic conditions (F and G) but not under neutral conditions (H and I). The differences in urease activities (J–M) implied that Bi inhibited the enzyme function. (*, p < 0.05).