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Protective effect of simvastatin on arterial plaque instability induced by p-cresyl sulfate.
European Review for Medical and Pharmacological Sciences 2018 September
OBJECTIVE: To study the protective effect of simvastatin on arterial plaque instability induced by p-cresyl sulfate (PCS).
MATERIALS AND METHODS: Apolipoprotein E (ApoE)-/- mice were selected as objects of this study. All mice were randomly divided into three groups: 1) the control group, 2) the PCS group and 3) the PCS + simvastatin group. After successful modeling, the levels of plasma cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein, interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-β (TNF-β) were detected. The gross specimen of coronary artery was stained. Meanwhile, oil red O staining and Sirius red staining were performed for coronary arterial sections to observe the lipid and collagen components. The expression levels of smooth muscle cells and macrophages were observed by immunohistochemistry. In addition, the expression levels of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs) and monocyte chemoattractant protein-1 (MCP-1) in tissues were detected by Western blotting.
RESULTS: Simvastatin could improve atherosclerotic plaque growth and atherosclerotic plaque instability induced by PCS. Moreover, simvastatin could also improve the changes of MMPs and TIMPs caused by PCS as well as the inflammatory status in mice.
CONCLUSIONS: Simvastatin can improve the inflammatory status in mice, eventually improving the arterial plaque instability caused by PCS.
MATERIALS AND METHODS: Apolipoprotein E (ApoE)-/- mice were selected as objects of this study. All mice were randomly divided into three groups: 1) the control group, 2) the PCS group and 3) the PCS + simvastatin group. After successful modeling, the levels of plasma cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein, interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-β (TNF-β) were detected. The gross specimen of coronary artery was stained. Meanwhile, oil red O staining and Sirius red staining were performed for coronary arterial sections to observe the lipid and collagen components. The expression levels of smooth muscle cells and macrophages were observed by immunohistochemistry. In addition, the expression levels of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs) and monocyte chemoattractant protein-1 (MCP-1) in tissues were detected by Western blotting.
RESULTS: Simvastatin could improve atherosclerotic plaque growth and atherosclerotic plaque instability induced by PCS. Moreover, simvastatin could also improve the changes of MMPs and TIMPs caused by PCS as well as the inflammatory status in mice.
CONCLUSIONS: Simvastatin can improve the inflammatory status in mice, eventually improving the arterial plaque instability caused by PCS.
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