Objective To investigate the in vitro inhibitory and bactericidal activities of the trans-2-decenal compound against Helicobacter pylori (H. pylori) and explore its potential mechanism.

Methods The minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) of trans-2-decenal against H. pylori clinical isolates and the standard strain ATCC 43504 were determined using the broth microdilution method. Changes in MIC values were monitored to assess drug resistance in H. pylori induced by continuous treatment with trans-2-decenal. The synergistic antibacterial effect of combining trans-2-decenal with antibiotics such as metronidazole (MTZ), clarithromycin (CLA), amoxicillin (AMX), and levofloxacin (LEV) was evaluated using the fractional inhibitory concentration index (FICI). After treating standard H. pylori strains with trans-2-decenal, scanning electron microscopy, transmission electron microscopy, crystal violet staining, the semi-solid puncture method, and the Berthelot method were used to assess the effects of trans-2-decenal on the morphology, cell structure, migration, and urease activity of H. pylori.

Results The MIC range for clinically resistant H. pylori strains C907, C101, R1, R2, R4, R10, R16, R24, R36, and R40 was 8-16 μg/mL, with an MBC range of 16-32 μg/mL. The MIC for the H. pylori standard strain ATCC 43504 was 16 μg/mL, with an MBC of 16 μg/mL.Trans-2-decenal inhibits H. pylori at low concentrations for short durations and does not easily induce H. pylori resistance. Trans-2-decenal reduces the required dosage of antibiotics (metronidazole and levofloxacin), showing an additive effect. Trans-2-decenal alters the shape of H. pylori and promotes bacterial rupture. Furthermore, Trans-2-decenal exerts its effects by altering H. pylori morphology, inducing bacterial rupture, inhibiting biofilm formation, reducing the number of mature biofilms, and decreasing urease activity and H. pylori migration ability.

Conclusion Trans-2-decenal may inhibit H. pylori in vitro through multiple mechanisms and is unlikely to promote the development of H. pylori resistance.