BECAS
SALINAS IBAÑEZ Angel Gabriel
congresos y reuniones científicas
Título:
Effects of Origanum vulgare (oregano) on the response of Helicobacter pylori to oxidative stress
Autor/es:
AGUILAR LUCERO D, ; SALINAS IBÁÑEZ AG, ; FERRAMOLA FF; ARISMENDI SOSA AC, .; VEGA AE
Lugar:
San Luis
Reunión:
Congreso; XXXII Reunión Anual de la Sociedad de Biología de Cuyo.; 2014
Institución organizadora:
Sociedad de Biología de Cuyo
Resumen:
Helicobacter pylori is a microaerophilic, gram-negative human pathogen that causes several gastricpathologies.Despitethe chronic gastritis that develops, the microorganism is able topersist in the stomach fordecades.H. pylori produces a strong immune response. The oxidative burst with production of reactive oxygenspecies (ROS) contributes to the microbicidalactivity of macrophages. H. pyloriis able to protect itself from ROSthrough induction of antioxidant enzymes such as superoxide dismutase (SOD). The bacterial attachment tostomach epithelium is the initial step for the pathogenesis and H. pylori has the capacity to form biofilm. In thisstate, H. pyloriexhibits a remarkable protection against antimicrobial agents.Many therapeutic agents are used forits eradication, however, the increase of resistant strains leads to the search of herbs and spices with antimicrobialpotential against H. pylori. In this study, the effect of oregano on the expression of sod gene in H. pyloriplanktonic cells and biofilm was evaluated. The reference strain NCTC146128 was grown in Petri dish withMueller-Hinton broth plus 5% fetal calf serum and 0.3% glucose, and a glass surface for adherence and formationof biofilmwas added. The culture was incubated in microaerophilia for 72 h at 37ºC. Then,the biofilm wastransferred to a new plate with medium added with 1 mg/ml of oregano extract and was incubated for 26h.ForRNA extraction, the biofilm and planktonic cells were treated with Trizol, and cDNA was obtained. Oreganosignificantly suppressed the expression of sodgene in both states.The results suggest that oregano could exert aprotective effect inhibiting the sod-dependentantioxidant mechanismwherebyH. pylorisurvives inmacrophages.These pathways represent potential targets for therapeutic exploitation.