MDG-1 inhibits H2O2-induced apoptosis and inflammation in human umbilical vein endothelial cells

Abstract

MDG-1, a water-soluble polysaccharide extracted from Ophiopogon japonicus, has been reported to serve a role in antimyocardial ischemia by protecting cardiomyocytes from hypoxia/reoxygenation-induced damage. However, it remains unknown whether MDG-1 protects human umbilical vein endothelial cells (HUVECs) against oxidative stress-induced damage. In the present study, HUVECs were treated with hydrogen peroxide (H2O2) to establish an oxidative stress-induced cell injury model. Treatment of HUVECs with different concentrations of H2O2 significantly attenuated cell viability and increased cell apoptosis in a time and dose-dependent manner. Pretreatment with MDG-1 markedly reduced H2O2-induced cell death, ROS generation and inflammatory factor secretion. In addition, pretreatment with MDG-1 decreased the expression levels of proapoptotic proteins BCL2 associated X (Bax) and caspase-3, while it increased the expression levels of the antiapoptotic protein BCL2 apoptosis regulator (Bcl-2), compared with H2O2 treatment alone. Taken together, the present data suggest that MDG-1 protected HUVECs against H2O2-induced apoptosis and inflammation through inhibition of Bax/Bcl-2 protein ratio, caspase-3 expression, and inflammatory factor secretion. This study provides a potential application for MDG-1 in the treatment of cardiovascular disease.