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摘要Background Epidemiological studies have shown apple polyphenols (APs) can decrease the risk of metabolic diseases and cardiovascular disease (CVD) by lowering levels of low-density lipoprotein (LDL) and total cholesterol.As a mixture of various antioxidants, APs are widely investigated for the protective effects against oxidative stress.However, it is unclear whether they are beneficial in the onset and progression of atherosclerosis.Methods Here we first observed that lipopolysaccharide (LPS) increased the levels of monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in cultured rat aortary endothelial cells (RAECs) in a time-and concentration-dependent manner.Then we tested the effects of APs on the endothelial activation and monocyte adhesion to RAECs induced by LPS.RAECs were pretreated with various concentrations (1-100 μg · mL-1~) of APs prior to stimulation with LPS (100 ng · mL1) for 1 hour.Results APs diminished reactive oxidative species (ROS) production in activated endothelial cells due to their potent antioxidant capacity.Western Blot analyses showed that APs suppressed LPS-induced phosphorylation of p38 and ERK1/2, as well as degradation of I κ Bα and activation of nuclear factor-kappa B (NF-κ B) at concentrations ranging from 1 to 100 μg · mL-1.In consequence, the adhesion of peripheral blood mononuclear leucocytes (PBMLs) to LPS-stimulated RAECs was markedly prevented by APs.Conclusions and general significance The results demonstrated that APs protected endothelial cells from the LPS-induced atherosclerosis in vitro through regulating the leukocyte recruitment and endothelial activation.Diets supplemented with apple polyphenols could exercise a significantly higher positive influence on atherosclerotic lesion formation.