title: Atorvastatin attenuates p‑cresyl sulfate‑induced atherogenesis and plaque instability in ApoE knockout mice.
abstract: p-cresyl sulfate (PCS) is a protein-bound uremic toxin retained in the blood of patients with chronic kidney disease (CKD) As atherosclerosis is a primary cardiovascular complication for patients with CKD, the aim of the present study was to investigate the mechanisms underlying the aggravation of atherosclerosis by PCS. In addition, the effect of atorvastatin was assessed in reversing the effects of PCS. PCS was revealed to promote the initiation and progression of atherosclerosis. Following treatment with atorvastatin, apolipoprotein E knockout mice demonstrated a reduction in PCS‑induced atherogenesis and plaque vulnerability. In addition, atorvastatin decreased the protein expression levels of vascular cell adhesion molecule‑1 and intercellular cell adhesion molecule‑1, and the interaction between leukocytes and endothelia. The plasma lipid profiles of mice were not significantly affected by gavage of low‑dose atorvastatin. The results of the present study indicate that PCS promotes plaque growth and instability by enhancing leukocyte‑endothelium interaction, and that these effects may be attenuated by atorvastatin treatment.
authors: Department of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors: Hui
authors: H
authors: Han
authors: Department of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors: Yanjia
authors: Y
authors: Chen
authors: Department of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors: Jinzhou
authors: J
authors: Zhu
authors: Department of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors: Jingwei
authors: J
authors: Ni
authors: Department of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors: Jiateng
authors: J
authors: Sun
authors: Department of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.
authors: Ruiyan
authors: R
authors: Zhang
mesh_terms: D000818:Animals; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D001011:Aorta / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics*; D050197:Atherosclerosis / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D000069059:Atorvastatin / Q000627:therapeutic use*; D003094:Collagen / Q000032:analysis; D003408:Cresols; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008297:Male; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D058226:Plaque, Atherosclerotic / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D013463:Sulfuric Acid Esters; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
chemical_list: D000924:Anticholesteremic Agents; D001057:Apolipoproteins E; D003408:Cresols; D013463:Sulfuric Acid Esters; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; C408690:4-cresol sulfate; D003094:Collagen; D000069059:Atorvastatin