细颗粒物PM2.5,脉粥样硬化,基因敲除,动物实验 z-bo 2020-09-14 356

　　Objective This experiment aims to investigate the effect and mechanism of fine particulate matter PM2.5 (PM2.5) on ApoE gene knockout (Apoe-/-) mice (atherosclerosis model mice).

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

　　Results The content of heavy metals in the whole blood of the PM2.5 group mice increased (P<0.05), the="" heart="" function="" did="" not="" change="" significantly="" p="">0.05), the blood glucose and blood lipid levels were not significantly different (P>0.05), and the serum inflammatory factor levels increased significantly 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 Apoe-/- atherosclerosis in mice, and the mechanism may be related to inflammation and oxidative stress.