Abstract
Purpose: To elucidate the anti-atherosclerotic effect of Yerba Mate polyphenols (MP) as well as the anti-atherosclerotic effect of a combination of MP and silencing of lectin-like oxidized low-density lipoprotein receptor-1 interference group (LOX)-1.Methods: The anti-atherosclerotic effects of control group (CG), simvastatin group (SG), MP group (MP), LOX-1 interference group (LOX) and MP + LOX-1 interference group (MP-LOX) were determined using Oil Red O staining, enzyme-linked immunosorbent assay (ELISA) and Western blot assay.Results: The levels of foam cells, intracellular lipids, viz, total cholesterol (TC), free cholesterol (FC), cholesterol ester (CE) and acyl-coenzyme A: cholesterol acyltransferase 1 (ACAT1); LOX-1, inflammation (TNF-alpha, IL-6 and pNF-κB/NF-κB); adhesion molecular status (ICAM-1 and VCAM-1), and monocyte chemotactic protein-1 in SG and in MP, LOX and MP-LOX groups were significantly decreased, when compared with CG (p < 0.01). The levels of these parameters were much lower in MPLOX group than in SG (p < 0.01). However, they were synergistically reduced in MP-LOX group, relative to MP group or LOX group (p < 0.01). Combination of LOX-1 gene silencing with MP produced synergistic anti-atherosclerotic effect which was reflected in decreases in foam cell formation, intracellular lipids, inflammatory status, adhesion molecular status, and MCP-1-mediated migration and infiltration of macrophages in foam cells.Conclusion: The synergistic anti-atherosclerotic effects of MP and LOX-1 gene silencing may be potential tools for development of anti-atherosclerotic agents.
Highlights
Macrophage-derived foam cells (MFC) which are chief cellular components of atherosclerotic plaques, are involved in two major pathogenic processes in atherogenesis: cholesterol buildup and inflammatory status [1,2]
Results from Oil Red O staining showed that the PMA- and oxidized low-density lipoprotein (ox-LDL)-induced foam cell formations were successfully established in control group (CG)
Numerous deep red-stained lipid droplets were present in cytoplasm, and the lipid content exceeded 60 % in most cells, indicating that the foam cell model was successfully established in CG
Summary
Macrophage-derived foam cells (MFC) which are chief cellular components of atherosclerotic plaques, are involved in two major pathogenic processes in atherogenesis: cholesterol buildup and inflammatory status [1,2]. Acyl-Coenzyme A: cholesterol acyltransferase 1 (ACAT1) is an intracellular enzyme that converts free cholesterol (FC) into cholesteryl esters (CE) for storage in lipid droplets, and it promotes foam cell formation in atherosclerotic lesions [5,6]. Several studies have shown that simvastatin therapy is associated with harmful side effects [16,17] It is still unknown whether MP inhibits foam cell formation in atherosclerosis, nor are the molecules and signaling pathways involved known. The slides of foam cells were washed three times with phosphate buffer saline (PBS), and traces of water were blotted, followed by fixation in 10% neutral formaldehyde for 10 min, and Oil Red O staining for 10 min.
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