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 line. 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 qPCR.
Results PHI inhibited the growth of Hp, 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, qPCR and Western blotting results revealed that PHI significantly suppressed the upregulation of VASN mRNA and protein expression in GES-1 cells induced by Hp. Further qPCR results showed that PHI inhibited Trx mRNA expression in Hp.
Conclusions 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.
DownLoad: