Objective To explore the effects of Phillygenin (PHI) on the infection of human gastric epithelial cells GES-1 by Helicobacter pylori (Hp) and the expression of its virulence factor cytotoxin-associated protein A (CagA), and to elucidate the role of the Vasorin (VASN)/Thioredoxin (Trx) axis in this process.

Methods Experiments were conducted using standard Hp strains and human gastric mucosal GES-1 cell lines. The minimal inhibitory concentration (MIC) of PHI was determined through MIC experiments. An Hp infection model was established in GES-1 cells. Cell viability was assessed using the CCK-8 assay, apoptosis levels were detected using Annexin V-FITC/PI double staining by flow cytometry, and CagA and VASN protein levels in GES-1 cells were measured using Western blotting. VASN mRNA expression in GES-1 cells and Trx mRNA expression in Hp were detected by realtime-PCR.

Results PHI inhibited the growth of Hp in a dose-dependent manner, with an MIC value of 4 μg/mL. The CCK-8 assay results showed that PHI significantly counteracted the inhibitory effect of Hp on GES-1 cell viability. Flow cytometry results indicated that PHI significantly reduced the apoptosis rate of GES-1 cells induced by Hp. Western blotting results demonstrated that PHI inhibited the delivery of the virulence factor CagA from Hp to GES-1 cells. Additionally. Realtime-PCR and Western blot results revealed that PHI significantly suppressed the upregulation of VASN mRNA and protein expression in GES-1 cells induced by Hp. Further realtime-PCR results showed that PHI inhibited Trx mRNA expression in Hp.

Conclusion PHI can inhibit the growth of Hp and the expression of its virulence factor CagA, reducing infection-induced damage to gastric epithelial cells. This process may be mediated through the regulation of VASN and Trx, providing a new theoretical basis for the development of anti-Hp drugs.