动物造模,慢性胃炎模型 z-bio 2021-05-10 749

　　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 method to establish in vivo infection, 2 weeks after infection, use 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, gastric gland tissues were collected for HE and methylene blue borate staining to analyze the degree of gastritis and Helicobacter pylori infection. Biochemical methods are used to detect myeloperoxidase (MPO) and superoxide dismutase (SOD) in gastric tissue. , 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, glandular atrophy and intestine. I will. 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 (P\u003c0.05). Or P\u003c0.01).

　　Conclusion: H. pylori can be successfully colonized in mice by oral administration, and may cause chronic inflammatory cell infiltration and increase gastric gland oxidation after 6 and 12 weeks of colonization. In the 12-week model, the stress level and pro-inflammatory expression genes have deeper infectivity, accompanied by gland atrophy and intestinal metaplasia.