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Introduction Exposure to the fine particulate matter PM2.5 is strongly associated 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 divided 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 descending arteries were stained with oil red O; Aortic roots were stained with Movat, 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, consistent 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 macrophages (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 atherosclerosis in apoE –/– mice.

Introduction: Exposure to the fine particulate matter PM2.5 is strongly associated 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 divided 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 descending arteries were stained with oil red O; Aortic roots were stained with Movat, 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, consistent 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 macrophages (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 atherosclerosis in apoE-/- mice. [ABSTRACT FROM AUTHOR]