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本研究的目的在于用人类复合性溃疡患者幽门螺杆菌新鲜分离株感染BABL c小鼠建立动物胃炎模型。幽门螺杆菌 (H pylori)是由Warren和Marshall在 1989年首次发现的 ,此杆菌与胃炎和消化性溃疡相关联 ,从而彻底改变了对胃、十二指肠疾病的认识。 1990年澳大利亚国际胃肠病学术会议确认H pylori是导致胃炎的重要病因 ,由此引起的胃炎是发病率最高的消化性疾病 ,但仍有许多方面了解不够或有不同认识 ,存在的主要问题是缺乏简单、易控制的动物模型。我们选用复合性溃疡患者的幽门螺杆菌临床新鲜分离株 ,在微需氧条件下进行培养传代 ,然后按照 10 9集落形成单位 mL的菌量接种BALB c小鼠 ,接种前将小鼠禁食 2 4小时 ,并用 0 2 5mL 10 %NaHCO3 稍微中和胃部酸性 ,15分钟后接种 ,并于第 3、5天分别重复接种。于最后一次接种后 5天 ,2 ,3,4周分批处死动物 ,取出小鼠接近幽门部的胃粘膜组织 ,一部分用于H pylori鉴定 ,另一部分用于病理学检测。结果表明 ,接种幽门螺杆菌的实验组小鼠胃粘膜能分离出幽门螺杆菌 ,病理切片显示实验组小鼠胃粘膜有不同程度的胃炎 ,而空白对照组小鼠则无明显的炎症表现。从而建立了用人类复合性溃疡患者幽门螺杆菌新鲜分离株感染BALB c小鼠的动物胃炎模型。该模型可用于临床用药的筛选和
The aim of this study was to establish an animal model of gastritis by infecting BABL c mice with fresh H. pylori isolates from patients with human complex ulcer. H pylori, first discovered by Warren and Marshall in 1989, has been linked to gastritis and peptic ulcer disease, completely changing the understanding of gastric and duodenal diseases. 1990 International Symposium on Gastroenterology in Australia confirmed H pylori is an important cause of gastritis, the resulting gastritis is the highest incidence of digestive diseases, but there are still many aspects of inadequate or different understanding, the main problem is Lack of simple, easy to control animal models. We selected patients with complex ulcer of Helicobacter pylori fresh clinical isolates, cultured and subcultured under microaerobic conditions, and then inoculated BALB c mice in a volume of 10 9 colony forming units mL, mice were fasted before inoculation 2 4 hours and gastric acidity was slightly neutralized with 0 2 5 mL of 10% NaHCO 3, inoculated after 15 minutes, and inoculated separately on days 3 and 5. Five days after the last inoculation, animals were treated in batches at 2, 3, and 4 weeks. Gastric mucosal tissues of mice near the pylorus were removed, one part was used for identification of H pylori and the other part was used for pathological examination. The results showed that Helicobacter pylori was isolated from the gastric mucosa of mice inoculated with H. pylori. The pathological sections showed that gastric mucosa in the experimental group had different degrees of gastritis, while the blank control group had no obvious inflammatory manifestations. Thus, an animal model of gastritis in BALB c mice infected with fresh Helicobacter pylori isolates from patients with human complex ulcer was established. The model can be used for clinical drug screening and