Physcion 8-O-β-Glucopyranoside Alleviates Oxidized Low-Density Lipoprotein-Induced Human Umbilical Vein Endothelial Cell Injury by Inducing Autophagy Through AMPK/SIRT1 Signaling.

Aim: Vascular endothelial cell dysfunction plays a crucial role in the initiation and development of atherosclerosis. Physcion 8-O-beta-glucopyranoside (PG), an anthraquinone extracted from Polygonum cuspidatum, has a number of pharmacological functions. The aim of this study was to elucidate the protective effects of PG against oxidized low-density lipoprotein (ox-LDL) in VECs. Methods and Materials: Human umbilical vein endothelial cells (HUVECs) were used as the in vitro model. Cell viability and apoptosis were, respectively, assessed by CCK-8 assay and Annexin-V/PI staining. Formation of autophagosomes was visualized by acridine orange staining, and the autophagy flux was tracked after infecting the cells with the mRFP-GFP-LC3 adenovirus. The expression levels of various apoptosis and autophagy-associated marker proteins were detected by Western blotting. Results: Pretreatment with PG protected the HUVECs from ox-LDL-induced apoptosis. In addition, PG promoted autophagy in HUVECs, which was responsible for its antiapoptotic effects. Finally, activation of AMPK/SIRT1 signaling was upstream of PG-induced autophagy. Conclusions: PG has potential pharmacological effects against oxidative damage-induced HUVEC injury through inducing AMPK/SIRT1-mediated autophagy.