Helicobacter pylori infection plays a crucial role in the pathogenesis of peptic ulcer and gastric cancer. The current proton pump inhibitor-based triple regimens or second-line therapies for the eradication of Helicobacter pylori face an increase in resistance problems, demanding a search for novel candidates. A new strategy for reduction of Helicobacter pylori infection is to interfere with the interaction between bacteria and target cells and to kill the bacteria but not target cells at the same time. By this approach, we found that the combination of anti-adhesion, antibacterial, antioxidant agents like sialic acid and catechins have a protective potential against Helicobacter pylori-induced gastric injury via a biphasic response in apoptosis and autophagy. The combination of sialic acid and catechins induced an upregulation in autophagy and a downregulation in apoptosis in the Helicobacter pylori-infected gastric epithelium and efficiently reduced gastric inflammation. It appears that a novel agent or a combination of several agents can be utilized to protect against Helicobacter pylori-induced gastric injury via the mechanism of upregulation of survival-related autophagy and downregulation of death-related apoptosis.