动物造模,小鼠慢性胃炎模型 z-bio 2021-10-07 531

　　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 establishes in vivo infection within 2 weeks after infection, and rapid urease and PCR methods are used 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, in order to analyze the degree of gastritis and Helicobacter pylori infection, gastric gland tissues were collected, stained with HE and methylene blue borate, and biochemical methods were used to inject myeloperoxidase (MPO) and superoxide dismutase into It has been produced in stomach tissue. SOD) has been detected. Changes in the levels of malondialdehyde (MDA) and catalase (catalase, CAT); T-qPCR expression changes of COX-2, iNOS, TNF-α and IL-1β genes in gastric tissue were detected.

　　Results: Compared with the normal group, the stomach tissues of the 6-week and 12-week model groups were colonized by Helicobacter pylori, and there were different degrees of chronic inflammatory cell infiltration, gland atrophy and intestinal lamina propria. Metaplasia; At the same time, the levels of CAT and SOD in tissues were significantly reduced, the levels of MPO and MDA were significantly reduced, and the expression of COX-2, iNOS, TNF-α, and IL-1β genes were significantly increased (Pu003c0. 05). Or P u003c0.01).

　　Conclusion: H. pylori can be successfully colonized in mice by oral administration. After 6 and 12 weeks of colonization, it can cause chronic inflammatory cell infiltration and increase gastric gland oxidation. In a 12-week model that included stress levels and pro-inflammatory genes, gland atrophy and intestinal metaplasia were more deeply infected.