Ginkgo biloba extract down‐regulates LOX‐1‐mediated endothelial dysfuntion: Involvement of P38‐NF‐κB signaling pathway

Oxidized low‐density lipoprotein (oxLDL) is a proatherogenic molecule that accumulates in the vascular wall and contributes to the pathogenesis of vascular dysfuntion.LOX‐1, a lectin‐like oxLDL receptor, is responsible for binding and uptake of oxLDL in endothelial cells. It has been well documented that the activation of LOX‐1 can stimulate the formation of ROS and initiate a cascade of redox‐sensitive singnaling events. Ginkgo biloba extract (GbE), extracted from the leaves of the Ginkgo biloba tree, has been well known about its benefits in cardiovascular and neurological system. In this study, incubation of primary human umbilical vein endothelial cell culture (HUVECs) with oxidized low‐density lipoprotein (oxLDL) was to examine whether GbE protects against oxLDL‐induced endothelial dysfuntion and the underlying mechanisms were explore. Our results showed that GbE reduced ROS production and up‐regulation of LOX‐1 caused by oxLDL. In addition, oxLDL enhances cyclooxygenase 2 (COX‐2) expression through p38 MAPK phosphorylation and consequent NF‐κB translocation. These oxLDL‐induced endothelial dysfuntion were ameliorated dose dependently by GbE. Findings from this study suggest that GbE prevent oxidized LDL‐induced endothelial dysfuntion through down‐regulation of LOX‐1‐mediated singaling implying that GbE has a potential ability in the prevention of atherosclerotic vascular disease.