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Astaxanthin decreases inflammatory biomarkers associated with cardiovascular disease in human umbilical vein endothelial cells

As a potent antioxidant, astaxanthin may downregulate inflammation‐associated factors involved in endothelial dysfunction and cardiovascular disease progression. We studied the possible protective effects of astaxanthin against endothelial dysfunction in human umbilical vein endothelial cells (HUVEC) induced with H2O2. Cells were pre‐incubated with 0, 0.01, 0.1, or 1.0 μmol/L astaxanthin for 48 h, then oxidative stress induced with 100 μmol/L H2O2 overnight. Uptake kinetics showed a time‐dependent accumulation of astaxanthin (1.0 μmol/L) by HUVEC over the 48 h period. Oxidative stress induction with H2O2 decreased intracellular antioxidant activity (SOD and GPx) and increased the production of reactive oxygen species (ROS), inflammatory cytokines and mediators. In contrast, pre‐incubation of HUVEC with astaxanthin prior to H2O2 stress increased (P < 0.05) SOD, but not GPx activity, and decreased the production of ROS, PGE2, LTB4, NO, IL‐8, and IFN‐γ. Pre‐treatment with astaxanthin also downregulated transcriptional activation of NF‐κB and activator protein‐1, thereby inhibiting downstream production of inflammatory cytokines and mediators. Therefore, astaxanthin inhibits inflammatory biomarkers upregulated by H2O2, likely by scavenging ROS required for transcriptional activation. Supported by the University of Washington and Washington State University.