Abstract
Helicobacter pylori is a Gram-negative microaerophilic gastric pathogen that infects approximately one-half of the human population. Infection withH. pylori is associated with gastritis, ulcerations, and gastric cancer.The common therapy for H. pylori infections is triple therapy that includes two kinds of antibiotics and a proton pump inhibitor. Given the high use of the antibiotic treatment, there is a decreasing rate in eliminating the infection in most countries.Curcumin is a natural yellow coloring polyphenol agent present in the spice turmeric (Curcuma longa), exhibits anti-inflammatory, antineoplastic, anti-oxidant and chemopreventive activities and has been demonstrated the effects of curcumin on the serum cholesterol and lipid peroxide levels. The membrane of biological cells or intra-cellular organelles plays an important role in maintaining cellular physiological functions. Here we utilized curcumin to treat AGS cells to evaluate the change in the membrane fluidity and to evaluate whether internalized of H. pylori was influenced (H. pylori internalization) by curcumin treatment. Results from amoxicillin protection assay showed that there was reduced colony forming numbers of bacteria when cells were treated with curcumin. We also observed a higher level of amoxicillin in the cytosol for curcumin-treated cells. Finally we applied fluorescence correlation spectroscopy (FCS) that is a technique to study molecular dynamics and mobility at single molecule level in solution. Our results revealed that curcumin treated cells exhibited a higher diffusion coefficient than did cells without treatment. Our results together suggested that curcumin influenced the membrane fluidity, thereby bacterial internalization. We have also analyzed the effect of cholesteryl-α-D-glucopyranosides (αCGs) by cholesterol-α-glucosyltransferase on the membrane fluidity. We have prepared a fluorophore-labeld αCG –incorporated liposomes. Fluorescence correlation spectroscopy analysis revealed that the addition of αCGs into the liposome led to an increased value of diffusion coefficient of DiIC18. Our results revealed that αCGs-treated liposome or cells exhibited a higher diffusion coefficient than did cells without treatment. Our results together suggested that αCG influenced the membrane fluidity.