Helicobacter pylori eradication attenuates oxidative stress in human gastric mucosa.

摘要: OBJECTIVE: Helicobacter pylori infection causes gastric diseases, but the responsible mechanisms are not completely understood. They can involve DNA and tissue damage induced by reactive oxygen nitrogen species. Our aim is to investigate effects of bacterial eradication on oxidative stress measuring changes relevant markers. METHODS: Antral biopsies were obtained from 34 patients with chronic atrophic gastritis peptic ulcer disease before after eradication. The expression inducible nitric oxide synthase (iNOS) levels nitrotyrosine (NTYR) 8-hydroxy-2′-deoxyguanosine assessed immunohistochemically as markers (NO) production proteins DNA, respectively. RESULTS: Before treatment, percentages staining were: 56 for iNOS in inflammatory cells, 79 61 NTYR foveolar respectively, 82 lymphoid follicles. was associated intensity inflammation (p = 0.04) activity 0.07). prevalence tended be that NTYR. After successful H. eradication, (in mild gastritis) decreased < 0.001 p 0.06, respectively). 8-Hydroxy-2′-deoxyguanosine disappeared 24% cases appeared 18% previously negative despite eradication. CONCLUSION: Targets deep cells This first report localization mucosa. Oxidative reduced stages gastritis. Moderate-severe may a step reversible iNOS, partly irreversible 8-hydroxy-2′-deoxyguanosine.