Scope: Palmitic acid (PA) contributes to the pathogenesis of cardiovascular disease by promoting endothelial dysfunction, while naringenin, most abundant in oranges, has been shown to exert multiple beneficial effects on the human cardiovascular system. This study explores whether naringenin prevents PA-induced apoptosis in human umbilical vein endothelial cells (HUVECs).
Methods and results: Treatment of PA for at least 24 h causes observable decrease in levels of cell viability, oxidative stress, disorder of autophagy flux, and apoptosis in HUVECs. Naringenin enhances the viability of the PA-treated HUVECs and, additionally, effectively decreases oxidative stress by scavenging ROS, and increasing the SOD2 level and GPx activity. Autophagy flux is protected by naringenin, as evidenced by the decreases in the ratio of LC3B-II/I, expression level of p62 and number of autophagosomes, and the increase in the number of autolysosomes in the PA-induced HUVECs. These effects are confirmed by the oxidative stress inhibitor N-acetyl-cysteine and autophagy inhibitor chloroquine. The molecular data indicate that the protective effects of naringenin on autophagy flux may also be regulated via the JNK pathway, as verified via the application of JNK inhibitor SP600125.
Conclusion: These findings provide a possible mechanism by which naringenin prevents endothelial dysfunction and cardiovascular diseases.
Keywords: apoptosis; autophagy; human umbilical vein endothelial cells; naringenin; palmitic acid.
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