Abstract
Atherosclerosis and related cardiovascular diseases represent the greatest threats to human health, worldwide. Previous animal studies showed that selenium nanoparticles (SeNPs) and Na2SeO3 might have anti-atherosclerotic activity, but the underlying mechanisms are poorly elucidated. This study compared the anti-atherosclerotic activity of SeNPs stabilized with chitosan (CS-SeNPs) and Na2SeO3 and the related mechanism in a high-fat-diet-fed apolipoprotein E-deficient mouse model of atherosclerosis. The results showed that oral administration of both CS-SeNPs and Na2SeO3 (40 μg Se/kg/day) for 10 weeks significantly reduced atherosclerotic lesions in mouse aortae. Mechanistically, CS-SeNPs and Na2SeO3 not only alleviated vascular endothelial dysfunction, as evidenced by the increase of serum nitric oxide level and the decrease of aortic adhesion molecule expression, but also vascular inflammation, as evidenced by the decrease of macrophage recruitment as well as the expression of proinflammatory molecules. Importantly, these results were replicated within in-vivo experiments on the cultured human endothelial cell line EA.hy926. Overall, CS-SeNPs had a comparable effect with Na2SeO3 but might have more potential in atherosclerosis prevention due to its lower toxicity. Together, these results provide more insights into the mechanisms of selenium against atherosclerosis and further highlight the potential of selenium supplementation as a therapeutic strategy for atherosclerosis.
Highlights
Atherosclerotic cardiovascular diseases (CVD) are the leading cause of mortality and a major cause of morbidity and disability worldwide [1,2]
Monocytes are recruited from the blood into the intima, where they differentiate into macrophages and take up modified lipoproteins to become foam cells
The result of transmission electron microscope (TEM) showed that CS-selenium nanoparticles (SeNPs) were uniformly spherical in shape and no significant aggregation was seen (Figure 1a)
Summary
Atherosclerotic cardiovascular diseases (CVD) are the leading cause of mortality and a major cause of morbidity and disability worldwide [1,2]. Atherosclerosis (AS) is a chronic inflammatory disease of the arterial wall, characterized by the formation of plaques consisting of foam cells, immune cells, vascular endothelial cells (ECs), vascular smooth muscle cells (VSMCs), platelets, extracellular matrix, and a lipid-rich core with extensive necrosis and fibrosis of surrounding tissues. Monocytes are recruited from the blood into the intima, where they differentiate into macrophages and take up modified lipoproteins to become foam cells (the hallmark of early fatty streak lesions). The concerted actions of activated ECs, VSMCs, monocyte-derived macrophages, and lymphocytes result in the production of a complex paracrine milieu of cytokines, growth factors, and reactive oxygen species within the vessel wall, which perpetuates a chronic proinflammatory state and fosters atherosclerotic lesion progression
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
