动物造模,慢性胃炎模型 z-bio 2022-11-11 416

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

　　Method: The stomach was perfused with H Pylori SS1 strain was established to infect in vivo, and the infection success rate was detected by rapid urease method and PCR method 2 weeks after infection; After confirmed successful infection, the animals were kept for 6 weeks and 12 weeks respectively to establish H Animal model of chronic gastritis related to pylori. After the experiment, gastric gland tissues were taken for HE and methylene blue borate staining to analyze the degree of gastritis and H The degree of Pylori infection; The contents of myeloperoxidase (MPO), superoxide dismutase (SOD), malondialdehyde (MDA) and catalase (CAT) in gastric tissues were measured by biochemical method; Detection of COX-2, iNOS and TNF in Gastric Tissues by RT qPCR- α And IL-1 β Changes in gene expression.

　　Results: Compared with the normal group, H pylori was colonized, and chronic inflammatory cell infiltration, glandular atrophy and intestinal metaplasia were found in the mucosa to varying degrees; At the same time, the content of CAT and SOD in tissues decreased significantly, the level of MPO and MDA and COX-2, iNOS, TNF- α And IL-1 β Gene expression increased significantly (P<0.05 or P<0.01).

　　Conclusion: The method of intragastric administration of bacteria can successfully transform H Pylori was implanted in mice, and after 6 and 12 weeks of implantation, it could cause chronic inflammatory cell infiltration, and enhance the level of oxidative stress and the expression of proinflammatory genes in gastric gland tissue. However, at 12 weeks, the infection of the model was deeper, with gland atrophy and intestinal metaplasia.