Atorvastatin ameliorated PM2.5-induced atherosclerosis in rats.

Abstract

PM2.5 provokes atherosclerotic events. Atorvastatin presents anti-inflammatory and antioxidant activities, and may ameliorate PM2.5-induced atherosclerosis development. The purpose of this study was to investigate the cardiotoxic effect of fine particulate matter (PM_2.5) on atherosclerosis (AS) in rats, and the intervention effects of atorvastatin (ATO) on PM_2.5-induced AS development. AS model was established using 32 male Wistar rats through intraperitoneal injection of vitamin D3 combined with a high-fat diet (10% fat and 4% cholesterol). The rats were randomly divided into 4 groups: control group, PM_2.5-exposed group, ATO group, and ATO treated PM_2.5-exposed group. PM_2.5 increased levels of TC, TG, LDL, MDA, IL-6, and TNF-α, as well as decreased SOD levels. Besides, PM_2.5 also enhanced AI. After the treatment of ATO, most levels of various contents in serum, including TC, TG, LDL, MDA, IL-6, TNF-α, hS-CRP, and ox-LDL, significantly decreased compared to the PM_2.5-exposed group. Moreover, after the treatment of ATO, AI was significantly reduced compared to the PM_2.5-exposed group. In addition, PM_2.5 exacerbated the nuclear translocation and ATO resulted in an obvious decrease in PM_2.5-induced nuclear translocation. The present study suggests that PM_2.5 could induce oxidative damage and systemic inflammatory response in atherosclerosis model rats, while ATO could ameliorate PM_2.5-induced atherosclerosis development, possibly by lowering lipid, inhibiting inflammation, and suppressing oxidation.