动物造模,小鼠慢性胃炎模型 z-bio 2023-01-16 1069

　　Objective: To establish an animal model of Helicobacter pylori infection and evaluate the pathological changes of the gastric mucosa of Helicobacter pylori-related chronic gastritis.

　　Method: Oral Helicobacter pylori SS1 strain by gavage to establish in vivo infection, 2 weeks after infection, rapid urease method and PCR method to detect the success rate of infection. After confirming successful infection, continue feeding for up to 6 weeks. Every 12 weeks. An animal model of chronic gastritis associated with Helicobacter pylori. After the experiment, the gastric gland tissue was collected by HE and methylene blue borate staining to analyze the degree of gastritis and Helicobacter pylori infection, and biochemical methods were used to produce myeloperoxidase (MPO) and superoxide dismutase in the gastric tissue. SOD) is detected. ), changes in malondialdehyde (MDA) and catalase (catalase, CAT) content; changes in T-qPCR expression to detect COX-2, iNOS, TNF-α and IL-1β genes in gastric tissue.

　　Result: 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 different degrees of chronic inflammatory cell infiltration, gland atrophy, and intestine. Metaplasia; At the same time, tissue CAT and SOD levels were significantly reduced, MPO and MDA levels were significantly reduced, COX-2, iNOS, TNF-α and IL-1β gene expression were significantly increased. \u003c0.05 or P\u003c0.01).

　　Conclusion: H. pylori can be successfully colonized in mice by gavage, and may cause chronic inflammatory cell infiltration and promote gastric glandular tissue oxidation after 6 and 12 weeks of colonization. Stress levels and pro-inflammatory gene levels, but the infection is deeper in the 12-week model, accompanied by gland atrophy and abnormal intestinal development.