动物造模,幽门螺杆菌感染小鼠慢性胃炎模型 z-bo 2021-10-28 723

　　Objective: To establish an animal model of Helicobacter pylori infection and evaluate the pathological changes of gastric mucosa in chronic gastrointestinal inflammation associated with Helicobacter pylori.

　　 Method: H. pylori SS1 strain is gavaged to establish in vivo infection, 2 weeks after infection, rapid urea method and PCR method are used to detect the success rate of infection. After confirming successful infection, continue feeding for up to 6 and 12 weeks respectively. An animal model of chronic gastrointestinal tract related to Helicobacter pylori. After the experiment, collect gastric gland tissue, stain with HE and methylene borate, analyze the degree of gastrointestinal inflammation and Helicobacter pylori infection, and detect myeloperoxidase (MPO) and superoxide dismutase in gastric tissue by biochemical method . Methods (superoxide dismutase, SOD), malondialdehyde (MDA) and catalase (catalase, CAT) content changes; detection of COX-2, iNOS, TNF-α and IL-1β gene RT in gastric tissue -qPCR method expression changes.

　　 Results: Compared with the normal group, Helicobacter pylori colonization was observed in the stomach tissues of the 6-week and 12-week model groups, and the mucosal layer had varying degrees of chronic inflammatory cell infiltration, gland atrophy and visible intestinal dysplasia. At the same time, the levels of CAT and SOD in the tissues were significantly reduced, the levels of MPO and MDA were significantly reduced, and the gene expressions of COX-2, iNOS, TNF-α and IL-1β were significantly increased (P). \u003c0.05 or P\u003c0.01).

　　 Conclusion: H. pylori can successfully colonize mice through forced feeding, and may cause chronic inflammatory cell infiltration and promote gastric gland tissue oxidation at 6 and 12 weeks after colonization. A 12-week model with stress levels and pro-inflammatory gene expression showed deeper infections, atrophy of glands, and abnormal intestinal development.