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The aim of this paper is to investigate the effect of patchouli alcohol in enhancing Helicobater pylori's action in eradicating macrophages and its mechanism. H. pylori was co-cultured with macrophages at a ratio of MOI=100 in different concentrations of patchouli alcohol. The effect of patchouli alcohol in eradicating macrophages was detected by agar dilution method. The effect of patchouli alcohol on NO and myeloperoxidase (MPO) levels in macrophages were measured by H. pylori by biochemical methods. Patchouli alcohol effect on H. pylori-induced pro-inflammatory gene expression and protein secretion in macrophages were detected by RT-qPCR and ELISA method. The eradication of H. pylori has significantly enhanced, and the destabilization of lysosomes has been reversed. Meanwhile, patchouli alcohol has an effect in inhibiting pro-inflammation and oxidation. The mechanism of patchouli alcohol in eradicating H. pylori and resisting oxidative stress may be associated to the blocking of bacteria escape lysosome combination procedures., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Chinese Pharmaceutical Association.)

This study further evaluated the in vitro and in vivo anti- Helicobacter pylori activities and potential underlying mechanism of patchouli alcohol (PA), a tricyclic sesquiterpene. In the in vitro assay, the capacities of PA to inhibit and kill H. pylori were tested on three standard strains at different pH values and on 12 clinical isolates. The effects of PA on H. pylori adhesion (and its alpA , alpB , and babA genes), motility (and its flaA and flaB genes), ultrastructure, and flagellation were investigated. Moreover, the H. pylori resistance to and postantibiotic effect (PAE) of PA were determined. Furthermore, the in vivo effects of PA on H. pylori eradication and gastritis were examined. Results showed that MICs of PA against three standard strains (pH 5.3 to 9) and 12 clinical isolates were 25 to 75 and 12.5 to 50 μg/ml, respectively. The killing kinetics of PA were time and concentration dependent, and its minimal bactericidal concentrations (MBCs) were 25 to 75 μg/ml. In addition, H. pylori adhesion, motility, ultrastructure, and flagellation were significantly suppressed. PA also remarkably inhibited the expression of adhesion genes ( alpA and alpB ) and motility genes ( flaA and flaB ). Furthermore, PA treatment caused a longer PAE and less bacterial resistance than clarithromycin and metronidazole. The in vivo study showed that PA can effectively eradicate H. pylori , inhibit gastritis, and suppress the expression of inflammatory mediators (COX-2, interleukin 1β, tumor necrosis factor alpha, and inducible nitric oxide synthase [iNOS]). In conclusion, PA can efficiently kill H. pylori , interfere with its infection process, and attenuate gastritis with less bacterial resistance, making it a potential candidate for new drug development., (Copyright © 2017 American Society for Microbiology.)