Ginsenoside Rg1 ameliorates apoptosis, senescence and oxidative stress in ox-LDL-induced vascular endothelial cells via the AMPK/SIRT3/p53 signaling pathway

Abstract

Coronary heart disease (CHD) mainly refers to coronary atherosclerotic heart disease and its pathogenesis is complex. Ginsenoside Rg1 (Rg1) has a wide range of pharmacological activities, such as antitumor effects, enhancing immunity and exerting protective effects on the vascular system. In the present study, the effect of Rg1 on vascular endothelial cells in CHD was investigated. Oxidized low-density lipoprotein (ox-LDL) was used to induce human umbilical vein endothelial cells (HUVECs) and cells were treated with 1, 5 or 10 µM Rg1. Cell Counting Kit-8 assay, TUNEL staining, western blot analysis of apoptosis-related proteins and senescence-related proteins, senescence-associated β-galactosidase staining, ELISA and other techniques including related kits of oxidative stress markers were used to detect the viability, apoptosis, oxidative stress, inflammatory cytokines including IL-1β, IL-6 and TNF-α and senescence of ox-LDL-induced HUVECs induced by Rg1. Western blot analysis was used to detect the expression levels of the AMP-activated protein kinase (AMPK)/sirtuin 3 (SIRT3)/p53 signaling pathway-related proteins. In addition, the associated mechanism was further determined using the AMPK pathway inhibitor compound C (CC). Rg1 increased the viability, and inhibited the apoptosis, senescence, oxidative stress and inflammation of ox-LDL-induced HUVECs. Pretreatment with CC partially reversed the protective effect of Rg1 on ox-LDL-induced HUVECs. In conclusion, Rg1 ameliorated apoptosis, senescence and oxidative stress of ox-LDL-induced HUVECs, at least in part, via the AMPK/SIRT3/p53 signaling pathway.