Abstract
BACKGROUND: Here, the study aims to explore the effect of PM2.5 exposure on atherosclerosis in rats. MATERIALS AND METHODS: 32 Wistar rats were selected in our study. An atherosclerosis model was established. All rats were evenly divided into four groups, including normal control group (NC), model control group (MC), model PM2.5 group (PM2.5) and model Atorvastatin group (Atorvastatin). The rats in NC and model control group were treated with saline 1 ml/kg body weight by tail intravenous injection, while the rats in PM2.5 group were exposed to PM2.5 suspension. The rats in atorvastatin group were given atorvastatin by gavage with 10 mg·kg(-1)·per day for 12 weeks until PM2.5 injection. After 24 h, all rats in each group were sacrificed. Pathological analysis, immunohistochemistry (IHC) and electrophoretic mobility shift assays (EMSA) were carried out. RESULTS: PM2.5 exposure significantly reduced the levels of triglyceride (TG), high density lipoprotein (HDL) and superoxide dismutase (SOD), but promoted the levels of total cholesterol (TC), low density lipoprotein (LDL), atherosclerosis index (AI), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) in the rats of PM2.5 group than MC group (p < 0.05). PM2.5 group showed activated nuclear factor-kappa B (NF-κB), seriously damaged myocardial coronary branches and the highest nuclear translocation rate. Atorvastatin significantly improved the levels of TG, HDL, SOD, interleukin-6 (IL-6), and reduced the levels of TC, LDL, AI, MDA, TNF-α, hs-CRP, oxidized low-density lipoprotein (ox-LDL) and blood pressure, even the nuclear translocation rate. CONCLUSIONS: PM2.5 exposure contributes to atherosclerosis in rats, which correlate with the levels of cholesterol, oxidative stress and inflammatory response. Atorvastatin could attenuate myocardial inflammation caused by PM2.5 exposure in rats.