Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2

Vessel endothelium injury caused by reactive oxygen species (ROS) including H(2)O(2) plays a critical role in the pathogenesis of cardiovascular disorders. Therefore, agents or antioxidants that can inhibit production of ROS has highly clinical values in cardiovascular therapy. Curculigoside is the major bioactive compounds present in Curculigo orchioides, and possess potent antioxidant properties against oxidative stress insults through undefined mechanism(s). The present study was designed to test the hypothesis that curculigoside can inhibit H(2)O(2)-induced injury in human umbilical vein endothelial cells.

Human umbilical vein endothelial cells (HUVECs) were treated with curculigoside in the presence/absence of hydrogen peroxide (H(2)O(2)). The protective effects of curculigoside OP-D against H(2)O(2) were evaluated.

HUVECs incubated with 400 μM H(2)O(2) had significantly decreased the viability of endothelial cells, which was accompanied with apparent cells apoptosis, the activation of caspase-3 and the upregulation of p53 mRNA expression. In addition, H(2)O(2) treatment induced a marked increase of MDA, LDH content and in intracellular ROS, decreased the content of nitric oxide (NO) and GSH-Px activities in endothelial cells. However, pretreatment with 0.5.5,10 μM curculigoside resulted in a significant recovery from H(2)O(2)-induced cell apoptosis. Also, it decreased other H(2)O(2)-induced damages in a concentration-dependent manner. Furthermore, pretreatment with curculigoside decreased the activity of caspase-3 and p53 mRNA expression, which was known to play a key role in H(2)O(2)-induced cell apoptosis.

The present study shows that curculigoside can protect endothelial cells against oxidative injury induced by H(2)O(2), suggesting that this compound may constitute a promising intervention against cardiovascular disorders.