Fig. 5: Amiodarone effectively prevented H. pylori from adhesion.

a Concentration–response plots of the inhibition against the CGAT-catalyzed hydrolysis of PE (14:0,14:0) (green) and the corresponding acyltransfer (blue). b Effect of amiodarone on the CAG formation in H. pylori. H. pylori 26695 cells were treated with amiodarone for 2 days, followed by LC-MS analysis. c–e Effects of amiodarone on H. pylori adhesion (c, d), CagA translocation, and CagA tyrosine phosphorylation (e). After treatment with amiodadrone, H. pylori 26695 or the mutant strain ΔCGAT was cultured with AGS cells for 1 h. Degree of adhesion was measured by flow cytometry analysis (c) and quantitated as the proportion of adhered cells with H. pylori (%, shown in each plot). The quantitation was summarized in (d). f–h Effects of amiodarone and OMVs on H. pylori adhesion (f, g), CagA translocation, and CagA tyrosine phosphorylation (h). AGS cells were treated with or without amiodarone in the presence of H. pylori 26695 OMVs (or the OMVs that had been pretreated with CAG(18:0)) for 8 h and then infected with H. pylori 26695 for another 1 h. f, g Degree of adhesion was shown in the same manner as c and d, respectively. i CAG levels in H. pylori 26695 and ten MDR strains clinically isolated. The bacterial strains were cultured for 2 days, followed by LC-MS analysis. j Effect of amiodarone on the CAG formation (shown by LC-MS analysis) in MDR 5024 strain. k, l Effects of amiodarone on the adhesion of MDR 5024 (k), CagA translocation, and the tyrosine phosphorylation (I). After treatment with amiodarone, MDR 5024 infected AGS cells for 1 h. In j–l, MDR+I denoted the incubation of MDR 5024 with amiodarone. In b, d, g, j and k, all statistically significant differences are indicated with asterisks; ***p < 0.001, **p < 0.01, *p < 0.05 vs. the control group (n = 3). In a–d, g, i–k, data are shown as mean ± SD, and provided in Supplementary Data 1. Uncropped immunoblot images for e, h, and l are provided in Supplementary Fig. 4.