Abstract
As society develops and aging populations increase, the incidence of arteriosclerosis, a seriously harmful cardiovascular disease (CVD) which mostly results from endothelial cellular oxidative damage, has continuously risen. Procyanidins from sea-buckthorn is a powerful antioxidant, although its protective effect on the cardiovascular system is not yet clearly understand. In this study, oxidative damaged HUVECs induced by palmitate acid (PA) were used as a model and the regulatory effect of procyanidins from sea-buckthorn (SBP) on HUVECs were investigated. The results showed SBP can be used for 12 h by HUVECs and had no detective cytotoxicity to them under 400 μg/L. Also, different concentrations of SBP can increase mitochondrial membrane potential and NO level and decrease LDH leakage in a dose-effect relationship, indicating SBP can improve oxidative damage. In addition, western blots and qPCR results showed SBP regulation on oxidative injured HUVECs is probably through p38MAPK/NF-κB signal pathway. This study revealed the molecular mechanism of procyanidins in decreasing endothelial oxidative damage, providing a theoretical foundation for further research on natural bioactive compounds to exert antioxidant activity in the body and prevent and improve cardiovascular diseases.