Objective To investigate the protective effect and its mechanism of edaravone against rat renal tubular epithelial cell injury induced by cisplatin. Methods The rat renal tubular epithelial cells (NRK-52E) were divided into the control, model control (50μmol·mL-1 cisplatin), group A (50μmol·mL-1 cisplatin plus 10μmol·mL-1 edaravone), B (50μmol·mL-1 cisplatin plus 20 μmol·mL-1 edaravone), and C (50 μmol·mL-1 cisplatin plus 40 μmol·mL-1 edaravone). The cell proliferation ability, content of malondialdehyde, activity of superoxide dismutase(SOD), level of reactive oxygen species ( ROS) , rate of apoptosis, express of protein and mRNA of Bax, Bcl-2 and Caspase-3 activation of cell were detected. Results The proliferation and SOD activity in NRK-52E cells declined, malondialdehyde and ROS were elevated upon being co-cultured with cisplatin. Moreover, the rate of apoptosis, express of protein and mRNA of Bax and Bcl-2, and Caspase-3 activation of cells were upregulated compared to the control group. However, edaravone stimulated cell proliferation, SOD activity and protein and mRNA of Bcl-2 and lowered content of malondialdehyde, level of ROS, rate of apoptosis, express of Bax protein and mRNA and Caspase-3 activation of cell(P<0. 05). Conclusion Edaravone can alleviate rat renal tubular epithelial cell injury induced by cisplatin, via inhibiting oxidative stress and down-regulating cell apoptosis.