Conclusion
These findings provide a possible mechanism by which naringenin prevents endothelial dysfunction and cardiovascular diseases.
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.