ABSTRACT
Helicobacter pylori infection is associated with chronic gastritis, peptic ulcers, and gastric cancer. The effects of Solanum lyratum extract (SLE) on anti-H. pylori activity and H. pylori-induced apoptosis were investigated. SLE showed a moderate ability in inhibiting growth of H. pylori and also in interrupting the association of bacteria with host cells. SLE was also able to suppress H. pylori-induced apoptosis. SLE inhibited caspase-8 activation, thereby preventing the release of cytochrome c from mitochondria and activation of the subsequent downstream apoptotic pathway. Thus, SLE may offer a new approach for the treatment of H. pylori by down-regulation of apoptosis in the H. pylori infected gastric epithelium. As it does not directly target bacteria, SLE treatment might not cause development of resistant strains.
Subject(s)
Apoptosis/drug effects , Helicobacter Infections/drug therapy , Helicobacter Infections/pathology , Helicobacter pylori/drug effects , Plant Extracts/pharmacology , Solanum/chemistry , Stomach Neoplasms/microbiology , Adenocarcinoma/drug therapy , Adenocarcinoma/microbiology , Adenocarcinoma/pathology , Cell Line, Tumor , Epithelial Cells/drug effects , Epithelial Cells/microbiology , Epithelial Cells/pathology , Helicobacter pylori/growth & development , Humans , Microbial Sensitivity Tests , Stomach Neoplasms/drug therapy , Stomach Neoplasms/pathologyABSTRACT
Helicobacter pylori infection is associated with an increased risk for development of duodenal ulcers, gastric ulcers, gastric adenocarcinomas and gastric lymphomas. However, resistant strains have developed because of antibiotic treatment. In this study, the water, acetone, chloroform and methanol extracts of two Solancaceae plants, Solanum erianthum and Solanum torvum (ST), were tested for their anti-H. pylori activity. All of ST extracts were able to inhibit the growth of H. pylori and showed better activities against antibiotic strains than the reference strain. Among them, chloroform extract of ST (ST-C) possessed the strongest ability to inhibit H. pylori growth. Association assay was performed by the ST-C showing that ST-C was able to interrupt the association of bacteria to host cells. Furthermore, H. pylori-induced apoptosis could also be efficiently suppressed by the ST-C. It was able to interfere with the interaction between bacteria and host cells and also target H. pylori-induced gastric injury by suppressing apoptosis. Therefore, ST-C may offer a new approach for the treatment of H. pylori. Further studies on the elucidation of the molecular mechanisms of the growth inhibition on H. pylori by ST-C, and to identify active compounds in the plants are in progress.
