Abstract
BACKGROUND The beneficial effect of Δ-17 FAD is poorly understood. The aim of this study was to investigate the protective mechanism of fatty acids against atherosclerotic (AS) damage induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs), and to identify the molecular mechanisms involved. MATERIAL AND METHODS The ox-LDL was used to induce lipotoxicity in HUVECs to establish a model of oxidative injury. HUVECs were transfected with Δ-17FAD lentivirus to induce cytoprotective effects. We evaluated the alterations in cell proliferation and apoptosis, and oxidative stress index, including levels of nitric oxide (NO), malonyldialdehyde (MDA), SOD enzyme, LDH, GSH-PX, and vascular endothelial growth factor (VEGF) expression. RESULTS The ox-LDL-induced excessive cellular apoptosis of HUVECs was abrogated by upregulation of Δ-17 FAD. Importantly, Δ-17 FAD converted ω-3 polyunsaturated fatty acid ARA into ω-6 polyunsaturated fatty acid EPA. Further, Δ-17 FAD overexpression promoted the proliferation of HUVECS, and inhibited ox-LDL-induced lipid peroxidation of HUVECs. The levels of nitric oxide, GSH-PX, and SOD enzyme were increased, and the activity of MDA and LDH was suppressed by the upregulation of Δ-17 FAD. In addition, upregulation of Δ-17 FAD significantly increased VEGF expression. In vitro tube formation assay showed that Δ-17 FAD significantly promoted angiogenesis. CONCLUSIONS These results suggest that Δ-17 fatty acid desaturase plays a beneficial role in the prevention of ox-LDL-induced cellular damage.