Ginsenoside Rg1 reduces toxicity of PM2.5 on human umbilical vein endothelial cells by upregulating intracellular antioxidative state

Ambient airborne particulate matter (PM) is an important environmental pollutant responsible for many human diseases. Oxidative stress is suggested to be involved in PM-induced cell injury. The present study is designed to study unsalutary effects of the organic extracts of PM with an aerodynamic diameter of less than 2.5 μm (PM2.5) and protective effect of Ginsenoside Rg1 (Rg1) against PM2.5 on human umbilical vein endothelial cells (HUVECs) in vitro. Cytotoxic effects of the organic extract PM2.5 on HUVECs were measured by means of HUVEC cell viability and the generation of intracellular reactive oxygen species (ROS). Expression of heme oxygenase-1(HO-1) and Nuclear factor-erythroid 2-related factor 2 (Nrf2) and Nrf2 cytoplasm–nucleus location were assayed. The present results showed that PM2.5 (50–800 μg/ml) decreased HUVEC viability and increased intracellular generation of ROS and malondialdehyde (MDA) in a concentration dependent manner, but increased HO-1 expression without concentration dependence. Rg1 (10 and 40 μg/ml) diminished PM2.5-induced HUVEC viability, decrease ROS and MDA generation, increased HO-1 and Nrf2 expression and promoted Nrf2 translocation to nucleus in a concentration dependent manner. These results suggested that organic extracts of PM2.5 increase oxidative stress and decrease cell viability; Rg1 antagonize PM2.5-induced excess oxidative stress; HO-1 expression increase and Nrf2 translocation to nucleus may be involved in the effects of both PM2.5 and Rg1 on HUVECs.

.Figure optionsDownload as PowerPoint slideHighlights
► PM2.5 increases generation of reactive oxygen species and decreases HUVEC viability.
► Rg1 antagonize PM2.5-induced excess oxidative stress within HUVECs.
► HO-1 expression increase and Nrf2 translocation to nucleus may be involved in the effects of Rg1.
► Rg1 may be a good agent to antagonize the unsalutary effects of PM2.5 on vascular endothelium.