动物造模,动脉粥样硬化,ApoE基因敲除小鼠 z-bio 2022-01-12 351

　　Purpose: This experiment aims to study the effect of particulate matter PM2.5 (particulate matter, PM2.5) on ApoE knockout (Apoe-/-) mice (atherosclerosis model mice) and its mechanism.

　　Methods: 328-week-old male Apoe-/- mice were divided into a normal control group (n = 16) and a PM2.5 group (n = 16) according to a random number table, and were given PM2.5 with a high/ -fat diet In the group, PM2.5 normal saline suspension (30 mg/(Kg/d)) was injected into the trachea at the same time, and the control group was injected with the same dose of normal saline. Eight weeks later, the heart function of the mice was evaluated, and the whole blood PM2.5 level, blood glucose level, blood lipid level, blood inflammatory factor level, blood reducing oil O staining and MOVAT were measured. I measured it. Aortic root staining was used to assess plaque area. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), lipoprotein-related phospholipase A2 (Lp-PLA2), NAD(P)H oxidase subunits p22phox and p47phox.

　　Result: The content of heavy metals in the whole blood of the PM2.5 group mice increased (P0.05), and there was no significant difference in blood glucose, blood lipid levels and serum (P\→0.05). The level of inflammatory factors was significantly increased (P\u003c0.05), atherosclerotic plaques were significantly increased (P\u003c0.05), IL-6, TNF-α, Lp-PLA2, P22phox and p47phox were expressed The level was significantly increased (P (u003c0.05).

　　Conclusion: PM2.5 exposure may accelerate the progression of atherosclerosis in Apoe-/- mice, and the mechanism may be related to inflammation and oxidative stress.