Ginsenoside Rb1 Prevents H2O2-Induced HUVEC Senescence by Stimulating Sirtuin-1 Pathway

Abstract

PurposesWe have previously reported that Ginsenoside Rb1 may effectively prevent HUVECs from senescence, however, the detailed mechanism has not demonstrated up to now. Recent studies have shown that sirtuin-1 (Sirt1) plays an important role in the development of endothelial senescence. The purpose of this study was to explore whether Sirt1 is involved in the action of Ginsenoside Rb1 regarding protection against H2O2-induced HUVEC Senescence.Methods and ResultsSenescence induced by hydrogen peroxide (H2O2) in human umbilical vein endothelial cells (HUVECs) was examined by analyzing plasminogen activator inhibitor-1 (PAI-1) expression, cell morphology, and senescence-associated beta-galactosidase (SA-β-gal) activity. The results revealed that 42% of control-treated HUVECs were SA-β-gal positive after treatment by 60 µmol/L H2O2, however, this particular effect of H2O2 was decreased more than 2-fold (19%) in the HUVECs when pretreated with Rb1 (20 µmol/L) for 30 min. Additionally, Rb1 decreased eNOS acetylation, as well as promoted more NO production that was accompanied by an increase in Sirt1 expression. Furthermore, upon knocking down Sirt1, the effect of Rb1 on HUVEC senescence was blunted.ConclusionsThe present study indicated that Ginsenoside Rb1 acts through stimulating Sirt1 in order to protect against endothelial senescence and dysfunction. As such, Sirt1 appears to be of particular importance in maintaining endothelial functions and delaying vascular aging.

Ginsenoside Rb1 inhibits free fatty acids-induced oxidative stress and inflammation in 3T3-L1 adipocytes

“…effects in diet-induced obese rats (15). Our recent study demonstrated that Rb1 pretreatment prevents human umbilical vein endothelial cell (HUVEC) senescence through modulation of the redox status and protects HUVECs from hydrogen peroxide (H 2 O 2 )-induced senescence through stimulation of the Sirtuin 1 pathway (16). However, limited data have been reported concerning the effect of Rb1 on FFA-induced inflammation in adipocytes.…”

β-elemene inhibits monocyte–endothelial cells interactions via reactive oxygen species/MAPK/NF-κB signaling pathway in vitro

“…In vitro experiments have sufficiently proved that oxidative stressors (e.g. H 2 O 2 and ox-LDL) could mimic the oxidative environment and lead to endothelial cells activation and elevation of adhesion molecule and chemokine expression (Song et al, 2014). H 2 O 2 can up-regulate CAMs' expression leading to monocytes adhesion to endothelial cells through the activation of NF-κB and MAPK signaling pathways and ultimately induce endothelial dysfunction .…”

Fermented Chinese Formula Shuan‐Tong‐Ling Protects Brain Microvascular Endothelial Cells against Oxidative Stress Injury

“…Research has found that SIRT1 can promote lifespan in higher organisms above yeast and metazoans [32], meanwhile promoting the protection of endothelial cells during oxidant stress exposure [14, 15]. Damaged mitochondria are thought to release more ROS and set in motion a vicious cycle of increasing DNA damage leading to increased ROS production that in turn leads to more DNA damage.…”

“…SIRT1 is an NAD-dependent deacetylase and modulates many biological processes, including oxidative stress, energy metabolism, cell differentiation, and genomic stability [13]. It has been reported that SIRT1 offered significant protection for cell survival in a number of disorders during oxidative stress [14, 15]. …”