Objective   To investigate the effects of delphinidin-3-glucoside (Dp-3-glc) on the oxidized injury

alteration of membrane potential and mitochondria potential

and p38MAPK phosphorylation of vascular endothelial cell line EA.hy926 induced by oxidized low density lipoprotein (Ox-LDL) and explore the molecular mechanism of the inhibitory effect of Dp-3-glc on endothelial oxidized injury.    Methods   Endothelial cells were preincubated for 2 h with Dp-3-glc at the concentrations of 25

50

100 or 200 μmol/L  and then treated for another 24 h with Ox-LDL of 100 μg/ml. MTT assay was used to detect the cell viability. MDA

LDH and NO in the supernatant and intracellular SOD activity were determined by the corresponding detection assay kits. Intracellular reactive oxygen species (ROS) production marked by DCFH-DA

membrane potential marked by DiSC3(5) and DiBAC4(3) and mitochondria potential marked by rhodamine-123 were respectively measured by laser confocal scanning microscopy. The phosphorylation level of p38MAPK was determined by Western blot assay.    Results   Preincubation with Dp-3-glc significantly inhibited Ox-LDL-induced reduction of cell viability

increase of MDA and LDH production

decrease of NO release and SOD activity

and intracellular ROS production in the endothelial cells. Ox-LDL obviously elevated the membrane potential

declined the mitochondria potential and increased the p38MAPK phosphorylation

while preincubation with Dp-3-glc inhibited the effects of Ox-LDL.    Conclusion   Dp-3-glc attenuates the Ox-LDL-induced stress injury in endothelial cells through decreasing the membrane potential and suppressing p38MAPK phosphorylation.