Quercetin Inhibits the Formation of Atherosclerosis Plaque by Protecting Vascular Endothelial Cells

Abstract

Background: Quercetin and its derivatives are the most widely distributed flavonoids, which have many pharmacological activities, such as anti-oxidation, anti-aging and anti-inflammatory, Quercetin inhibits the occurrence of atherosclerosis (AS) due to its antioxidant activity, but the mechanism is unknown. Results: Our research found that quercetin plays a role in reducing the formation of atherosclerotic plaque by protecting vascular endothelial cell injury. In an atherosclerotic mouse model, quercetin inhibited the formation of atherosclerotic plaques and downregulated the level of endothelial cell protein C receptors (EPCR), thrombomodulin (TM), von willabrand factor (vWF) and intercellular cell adhesion molecule-1(ICAM-1) in peripheral blood of AS mouse, because of increasing the number of vascular endothelial cells at the atherosclerotic plaque. In vitro model of human vascular endothelial cells (HUVECs) injury by H2O2, we found that quercetin significantly reduced endothelial cell apoptosis, and it can prevent vascular endothelial cell injury by inhibiting the secretion of chemokines (CXCL1 and CXCL8) and inflammatory (TNF-α, IL-β, IL-6 and IL-12) factors and reducing macrophage infiltration, at the same time, quercetin promotes the secretion of pro-angiogenic chemokines (CXCL4 and CXCL10) from vascular endothelial cells. Real-time PCR and western-blot assay found that the quercetin protects vascular endothelial cells by inhibiting apoptotic signaling pathway proteins (Bax and Bcl-2) and inflammatory regulatory pathway proteins (IκBα and p65). Conclusion: Consequently, we concluded that the role of quercetin in the protection of vascular endothelial cells against atherosclerotic plaques may be through the inhibition of vascular endothelial cell apoptosis.