Delphinidin-3-glucoside protects human umbilical vein endothelial cells against oxidized low-density lipoprotein-induced injury by autophagy upregulation via the AMPK/SIRT1 signaling pathway.

SCOPE: Oxidized LDL (oxLDL) induced vascular endothelial cell injury is a key event in the pathogenesis of atherosclerosis (AS). In our previous studies, we showed that delphinidin-3-glucoside (Dp), a natural anthocyanin, attenuated oxLDL-induced injury in human umbilical vein endothelial cells (HUVECs), indicating its potential role in preventing AS. However, the involved mechanism is not fully understood. METHODS AND
RESULTS: Via methyl thiazolyl tetrazolium and flow cytometry assay, we found that Dp-attenuated oxLDL-induced cell viability decrease and apoptosis in HUVECs. Depending on confocal microscopy, transmission electron microscopy, and Western blot assay, we found that Dp-induced autophagy in HUVECs, whereas suppression of autophagy significantly abolished the protective role of Dp against oxLDL-induced endothelial cell injury. Furthermore, Dp upregulated sirtuin 1 (SIRT1) expression and SIRT1 knockdown notably suppressed Dp-induced autophagy in HUVECs. Dp also increased the expression of phosphorylated adenosine monophosphate-activated protein kinase, while adenosine monophosphate-activated protein kinase (AMPK) knockdown remarkably abolished Dp-induced SIRT1 expression and subsequent autophagy.
CONCLUSION: Our data suggested that Dp protected HUVECs against oxLDL-induced injury by inducing autophagy via the adenosine monophosphate-activated protein kinase/SIRT1 signaling pathway. This new finding might shed light to the prevention and therapy of AS.