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Reactive Oxygen Species of Gastric Antral Mucosa in Patients with Peptic Ulcer Disease

消化性潰瘍病人胃竇部黏膜氣化自由基之探討

摘要


背景及目的:幽門桿菌感染與胃潰瘍及十二指腸潰瘍具有重要的相關性存在。幽門桿菌在胃黏膜誘發氧化自由基的生成,而胃黏膜氧化自由基在潰瘍之致病機轉中可能具有重要的角色。本研究之目的在於探討不同部位潰瘍病人胃竇黏膜氧化自由基之表現的差異性。 方法:本研究共收集45位消化性潰瘍病人(其中胃潰瘍18位,十二指腸潰瘍18位,合併十二指腸潰瘍及胃潰瘍9位),以內視鏡確定診斷潰瘍之部位。在胃竇黏膜部位做切片,然後以超微冷光(chemiluminescence)分析胃竇黏膜氧化自由基O2(上標 -)及H2O2。並對胃黏膜檢體進行蛋白質定量,校正超微冷光測定胃竇黏膜O2(上標 -)及H2O2,幽門桿菌感染以病理切片Hematoxylin-Eosin染色及Giemsa染色來確定。 結果:超微冷光利定胃竇黏膜之O2(上標 -)、H2O2,、蛋白校正之O2(上標 -)及H2O2在胃潰瘍、十二指腸潰瘍或合併二者病人身上並無統計上顯著之差異。但以病理診斷有無幽門桿菌感染分組(幽門桿菌感染陽性27位,陰性18位),在幽門桿菌感染組超微冷光所測得的H2O2及經蛋白質校正後的H2O2有顯著的上升。 結論:幽門桿菌確可導致胃竇黏膜氧化自由基的生成,且以H2O為主,但在不同部位潰瘍(胃或十二指腸),消化性潰瘍病人胃竇部氧化自由基的表現並無差異性存在。

並列摘要


Background and Objective: Researchers now have a better understanding of the mechanisms involving Helicobacter pylori (H. pylori) infection in peptic ulceration. H. pylori is considered to play a critical role in duodenal ulcers (DU) as well as gastric ulcers (GU). It also plays a key role in the production of reactive oxygen species (ROS) in gastric mucosa. However, the role of gastric antral mucosa ROS in patients with GU, DU or GU combined with DU (GU/DU) remains to be investigated. In this study, our aim was to determine the ROS by chemiluminescence (CL) assay of gastric antral mucosa in patients with peptic ulcer disease. Methods: Forty-five patients with GU, DU, or GU/DU (n=18, n=18, and n=9, respectively) were enrolled in this study. The diagnosis of peptic ulcer was based on the endoscopy presentation. Gastric mucosa specimens obtained from the gastric antrum for detection of O2(superscript -) or H2O2 activity were determined by CL assay. Protein concentrations in the tissue homogenates were determined by Bio-Rad protein assay. Results: There was no significant difference in amounts of O2(superscript -), H2O2, protein corrected O2 or H2O2 amounts among patients with GU, DU, or GU/DU. Results of CL assay revealed a significant difference in the amount of gastric antral mucosa H2O2 in peptic ulcer patients with H. pylori vs. those without H. pylori infection (H2O2 (counts/sec), 1512.67±747.97 vs. 342.39±205.40, p=0.045; H2O2 (counts/sec•μg), 43.79±22.30, 6.63±3.59, p=0.031). Conclusion: The role of H. pylori in the generation of ROS in gastric mucosa has been confirmed. In this study, we demonstrated that H. pylori increased H2O2 in gastric antral mucosa and there was no difference in gastric antral mucosa ROS between patients with GU, DU, and GU/DU.

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