Abstract: Objective To make sure whether the ERK1/2 signaling pathway plays an important role in aristolochic acid (AA) - induced the apoptosis of human umbilical vein endothelial cells (HUVECs). Methods Cell viabilities were determined by the MTT assays. Apoptotic morphologic changes of the treated cells were observed under fluorescence microscope. The proportions of apoptosis were assessed by flow cytometry. Western blotting was used to evaluate ERK1/2 phosphorylation. Results The MTT assays showed that AA significantly decreased the viabilities of HUVECs in a dose- and time-dependent manner. The flow cytometry showed that AA significantly increased the apoptosis of HUVECs in a dose-dependent manner. Microscopic apoptotic changes were also observed in these cells. Furthermore, AA inhibited ERK1/2 activation, which, however, was attenuated when the cells were pretreated with PD98095. A increase of apoptosis induced by AA was inhibited when the cells were pretreated with PD98095. Conclusion AA induces apoptosis of HUVECs via the ERK1/2 signaling pathway.

Key words: aristolochic acid, endothelial cell, apoptosis, ERK1/2 signaling pathway