Atorvastatin attenuates p-cresyl sulfate-induced atherogenesis and plaque instability in ApoE knockout mice

Autor: Jiateng Sun, Jinzhou Zhu, Jingwei Ni, Ruiyan Zhang, Hui Han, Yanjia Chen
Rok vydání: 2016
Předmět:
Male
0301 basic medicine
Apolipoprotein E
Cancer Research
medicine.medical_specialty
Atorvastatin
Intercellular Adhesion Molecule-1
uremic toxin
Vascular Cell Adhesion Molecule-1
Sulfuric Acid Esters
030204 cardiovascular system & hematology
Biochemistry
Cresols
03 medical and health sciences
Apolipoproteins E
0302 clinical medicine
p-cresyl sulfate
Internal medicine
Genetics
medicine
Animals
Cell adhesion
Molecular Biology
Aorta
Mice
Knockout
business.industry
Anticholesteremic Agents
Articles
atorvastatin
leukocyte-endothelium interaction
Atherosclerosis
medicine.disease
Molecular medicine
Plaque
Atherosclerotic
humanities
Mice
Inbred C57BL
030104 developmental biology
Endocrinology
Oncology
Apoptosis
Knockout mouse
Molecular Medicine
lipids (amino acids
peptides
and proteins)
Collagen
vulnerable plaque
business
Kidney disease
medicine.drug
Zdroj: Molecular Medicine Reports
ISSN: 1791-3004
1791-2997
DOI: 10.3892/mmr.2016.5626
Popis: 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.
Databáze: OpenAIRE
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