Abstract
ABSTRACTFas knockout (Fas−/-) mice are a model for systemic lupus erythematosus (SLE) -like autoimmune syndromes. We aimed to induce atherosclerosis (AS) in Fas−/- mice. Sixteen male Fas−/- mice were included in the study, sex-matched C57B6/L (B6) and apolipoprotein E-knockout (ApoE−/-) mice were negative and positive AS controls, respectively. A silica collar was placed around the right carotid artery of each mouse to induce AS development. All mice were fed a 24-week high-fat diet, and investigated for AS lesions. We also compared the levels of blood lipid and glucose, serum tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), anti-nuclear antibody (ANA) and anti-double-stranded deoxyribonucleic acid (anti-dsDNA) antibody in Fas−/- mice with those in B6 or ApoE−/- mice. All ApoE−/- and 6 Fas−/- but no B6 mice showed atherogenesis in right carotid artery. The carotid plaque contains more collagen and less lipid in Fas−/- than ApoE−/- mice. The levels of blood glucose, serum TNF-α, IL-6, ANA, and anti-dsDNA antibody were significantly higher in Fas−/- mice than those in B6 mice, the levels of serum TNF-α and blood glucose were significantly higher and the level of blood lipid was significantly lower in Fas−/- mice than those in ApoE−/- mice. Therefore, carotid AS can develop in Fas−/- mice. Fas−/- mice display higher levels of serum IL-6, TNF-α, ANA, and anti-dsDNA than B6 mice, higher levels of serum TNF-α and blood glucose and lower level of blood lipid than ApoE−/- mice, and less lipid and more collagen in AS plaque than ApoE−/- mice.
Published Version
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