Potential injurious effects of the fine particulate PM2.5 on the progression of atherosclerosis in apoE-deficient mice by activating platelets and leukocytes

Introduction: Exposure to the fine particulate matter PM2.5 is strongly as- sociated with atherosclerotic diseases, creating considerable public concern. Nevertheless, the mechanisms have not been fully elucidated. We exposed atherosclerosis-prone apoE-deficient mice to PM2.5 to begin investigating these mechanisms. Material and methods: Thirty-two 8-week-old male apoE–/– mice were divid- ed to two groups fed with high-fat diet: a control group instilled with 0.9% saline, and an experimental group instilled with PM2.5 (30 mg/kg/day) for 8 weeks. We measured PM2.5 in whole blood by the ICP-MS method, and lipids and inflammatory factors by standard methods. The whole descend- ing arteries were stained with oil red O; Aortic roots were stained with Mo- vat, Sirius Red and immunohistochemical stains for pathological analysis; Brachiocephalic arteries for scanning electron microscopy, the descending arteries for Q-PCR. Echocardiography was used to evaluate cardiac function. Results: In PM2.5 group, we observed elevated heavy metal components, con- sistent with higher amounts of platelets in total blood. The PM2.5 group also had elevated serum inflammatory factor levels. Finally, the PM2.5 group showed larger atherosclerotic plaques (p = 0.0231), higher numbers of lesion macro- phages (p = 0.0183), greater injury to endothelial layers with greater adherence of platelets and leukocytes, elevated inflammatory factor levels, the NAD(P)H oxidase subunits p22phox and p47phox (p = 0.0079 and p = 0.0294), the M1/ M2 associated markers IL-6, TNF-α (p = 0.0291, p = 0.0286), iNOS, IL-12 (p = 0.0122 and p = 0.0280) and arginase-1, and CD206 (p = 0.0216 and p = 0.0317). Conclusions: PM2.5 exposure activated circulating leukocytes, platelets and associated inflammatory factors, contributing to the progression of athero- sclerosis in apoE–/– mice.