Astaxanthin suppresses End MT by LOX-1 pathway in ox-LDL-induced HUVECs

Introduction Astaxanthin (ASX) is carotenoid with the highest antioxidant activity in various cell types and reverse atherosclerosis. However, roles detailed mechanisms of ASX atherosclerosis associated endothelial injury remains unclear. Methods In vitro model was established HUVECs by incubation oxidized low-density lipoprotein (ox-LDL). Cell viability oxidative stress were measured. The mRNA protein expressions lectin-like ox-LDL receptor (LOX-1) other related genes determined. Results reduced HUVECs, induced stress, as evidenced elevated cellular malondialdehyde (MDA) decreased superoxide dismutase (SOD). Pretreatment (50, 100, 200, 400 μM) markedly reversed reduction an increase migration (50 μg/mL). attenuated endothelial-to-mesenchymal transition (EndMT) process, increased CD31 α-SMA vimentin proteins treatment HUVECs. Furthermore, MDA decrease SOD ox-LDL, supernatant NO production, iNOS eNOS ox-LDL. enhanced (LOX-1), which dependent on ASX’s activity. inhibitory effect EndMT could be abolished overexpression LOX-1 Conclusions Our data speculate that prevents ox-LDL-induced inducing property (SOD NO) decreasing expression.