动物造模,基因敲除 z-bio 2022-09-26 442

　　Objective: To examine the effects of high-fat diet and K/BxN serum on the distribution of immune cells in ApoE knockout (ApoE-/-) mice

　　METHODS: ApoE-/- mice were fed a high-fat diet from 8 weeks of age and were injected intraperitoneally with anti-glucose-6-phosphateisomerase (GPI) antibody-positive K/BxN serum weekly at 17 weeks of age. One injection of 0.2 mL each time. The control group was fed with normal food. K/BxN serum was injected in the same way. Before and after the injection of K/BxN serum, the changes in blood lipid levels of mice were detected by ELISA. The degree of ankle joint swelling was measured by vernier calipers. The distribution of immune cells was analyzed by flow cytometry after the separation of spleen cells and bone marrow cells after treatment with BxN serum to 26 weeks of age.

　　Results: Serum low-density lipoprotein cholesterol (LDL-C) concentration, total cholesterol (TCHO) concentration and triglyceride ( TG) concentrations were significantly increased, and the plaque area at the root of the aortic valve was significantly increased, suggesting that regardless of whether K/BxN was injected with serum high-fat diet, ApoE-/- mice could develop arteriosclerosis symptoms and were significantly higher than ApoE-/- mice fed a normal diet. - Mice were more severely ApoE-/- mice before intraperitoneal injection of K/BxN serum ApoE-/- mice were at normal levels in ankle joint and arthritis clinical score after intraperitoneal injection of K/BxN serum and ApoE-/ on high-fat diet - The ankle joint width and arthritis scores of the mice were lower than those of the ApoE-/- mice fed a normal diet. The results of flow cytometry showed that the spleen and bone marrow of the ApoE-/- mice fed a high-fat diet were injected with K/BxN serum. CD3+ T cells and CD19+ B cells down-regulated CD11b+ macrophages up-regulated

　　CONCLUSION: High-fat diet and K/BxN serum cause down-regulation of CD3+ T cells and CD19+ B cells in the spleen and bone marrow of ApoE-/- mice and up-regulation of CD11b+ macrophages, leading to aggravation of arteriosclerosis symptoms and reduction of arthritis symptoms in ApoE-/- mice