动物造模,动脉粥样硬化 z-bio 2022-03-24 820

　　Objective The purpose of this experiment was to investigate the effect and mechanism of fine particulate matter PM2.5 on ApoE knockout (Apoe-/- ) mice (atherosclerosis model mice).

　　Methods Thirty-two 8-week-old male Apoe-/- mice were randomly divided into two groups: normal control group (n=16) and PM2.5 group (n=16). The PM2.5 group was instilled with normal saline suspension of PM2.5 (30mg/(Kg/d)) in the trachea, and the control group was instilled with the same dose of normal saline. After 8 weeks, the cardiac function of the mice was evaluated, the PM2.5 concentration in the whole blood, the blood glucose, blood lipid levels and inflammatory factor levels in the serum were measured, and the whole arterial oil red O staining of the descending artery and the MOVAT staining of the aortic root were used to evaluate the plaque area. Real-time fluorescence quantitative PCR method was used to detect tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), lipoprotein associated phospholipase A2 (Lp) in descending aorta. -PLA2), the levels of NAD(P)H oxidase subunits p22phox and p47phox.

　　Results The content of heavy metals in whole blood of mice in PM2.5 group increased (P<0.05), the="" cardiac="" function="" had="" no="" significant="" change="" p="">0.05), the blood glucose and lipid levels had no significant difference (P>0.05), and the serum inflammatory factor levels significantly increased. High (P<0.05), atherosclerotic plaques were significantly enlarged (P<0.05), and the expression levels of IL-6, TNF-α, Lp-PLA2, p22phox and p47phox were significantly increased (P<0.05).

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