BACKGROUND: Co-magaldrox (Maalox) is used world-wide as an antacid and as a cytoprotective agent for gastritis and peptic ulcer diseases. We examined the effects of co-magaldrox on Helicobacter pylori. METHODS: Adhesion of H. pylori to human gastric epithelial cells (MKN45) was evaluated by flow cytometry. Morphologic changes in H. pylori caused by co-magaldrox were determined by scanning electron microscopy. Induction of interleukin-8 (IL-8) from MKN45 cells was examined with enzyme-linked immunosorbent assay, and the intracellular and extracellular expression of heat-shock protein 60 (HSP60) was analyzed with sodium dodecyl sulphate-polyacrylamide gel electrophoresis and flow cytometry. RESULTS: Adhesion of H. pylori to MKN 45 cells was significantly inhibited by 1.25%-5% comagaldrox. H. pylori aggregated with co-magaldrox according to an electron microscopic examination. IL-8 secretion from MKN45 cells after H. pylori infection was also inhibited by co-magaldrox. Extracellular expression of HSP60 on the surface of H. pylori was decreased after treatment with comagaldrox, whereas the intracellular synthesis of HSP60 was not. HSP60-induced IL-8 secretion was significantly inhibited by co-magaldrox in a dose-dependent manner. CONCLUSIONS: These results show that co-magaldrox suppressed the expression of the following virulence factors: adhesion, IL-8 inducibility, and expression of extracellular HSP60. Therefore, co-magaldrox is a potent anti-H. pylori and cytoprotective drug.
BACKGROUND:Co-magaldrox (Maalox) is used world-wide as an antacid and as a cytoprotective agent for gastritis and peptic ulcer diseases. We examined the effects of co-magaldrox on Helicobacter pylori. METHODS: Adhesion of H. pylori to human gastric epithelial cells (MKN45) was evaluated by flow cytometry. Morphologic changes in H. pylori caused by co-magaldrox were determined by scanning electron microscopy. Induction of interleukin-8 (IL-8) from MKN45 cells was examined with enzyme-linked immunosorbent assay, and the intracellular and extracellular expression of heat-shock protein 60 (HSP60) was analyzed with sodium dodecyl sulphate-polyacrylamide gel electrophoresis and flow cytometry. RESULTS: Adhesion of H. pylori to MKN 45 cells was significantly inhibited by 1.25%-5% comagaldrox. H. pylori aggregated with co-magaldrox according to an electron microscopic examination. IL-8 secretion from MKN45 cells after H. pyloriinfection was also inhibited by co-magaldrox. Extracellular expression of HSP60 on the surface of H. pylori was decreased after treatment with comagaldrox, whereas the intracellular synthesis of HSP60 was not. HSP60-induced IL-8 secretion was significantly inhibited by co-magaldrox in a dose-dependent manner. CONCLUSIONS: These results show that co-magaldrox suppressed the expression of the following virulence factors: adhesion, IL-8 inducibility, and expression of extracellular HSP60. Therefore, co-magaldrox is a potent anti-H. pylori and cytoprotective drug.