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.