HDL inhibited atherosclerosis induced by radiation injury

Abstract

High-density lipoprotein (HDL) inhibits atherosclerosis development from radiation damage; nonetheless, the underlying mechanism is yet to be defined. This work studied patients treated with radiation along with cultured mouse aortic endothelial cells (MAECs) to investigate the process. Firstly, 158 patients who received radiation after neck cancers participated, and their arterial function was monitored by a B ultrasound. Similarly, HDL and other blood lipid indexes were also investigated. Then, MAECs were isolated, cultured, and passed through MTT assay to test the HDL protective role on ultraviolet B (UVB) radiation along with western blotting to test some apoptosis protein expression and possible molecules. Patients with high HDL levels were significantly less likely to develop atherosclerosis. We observed that MAECs treated with UVB were damaged significantly. However, HDL reversed the cell damage in a dose-depended manner. Meanwhile, the apoptosis process was investigated, and it revealed that HDL prevented UVB-induced apoptosis. Western blotting results showed that HDL enhanced phosphatidylinositol 3-kinase (PI3K) in addition to AKT phosphorylation in MAECs. These findings imply that HDL protects against UVB-induced apoptosis via activating the PI3K/AKT signaling pathway.