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.%目的：观察依达拉奉对大鼠肾小管上皮细胞的保护作用及其机制。方法将传代培养的大鼠肾小管上皮细胞(NRK-52E)分为对照组、模型对照组(50μmol·mL-1顺铂)、给药组A(50μmol·mL-1顺铂+10μmol·mL-1依达拉奉)、给药组B(50μmol·mL-1顺铂+20μmol·mL-1依达拉奉)和给药组C(50μmol·mL-1顺铂+40μmol·mL-1依达拉奉),检测各组细胞增殖能力、丙二醛( MDA)含量、超氧化物歧化酶( SOD)活性、活性氧( ROS)水平、细胞凋亡率、Bax和Bcl-2蛋白和mRNA表达以及Caspase-3活性。结果顺铂刺激NRK-52E细胞后,细胞增殖能力下降,MDA含量和ROS水平升高,SOD活性下降,细胞凋亡增加,Bax、Bcl-2蛋白和mRNA表达增多,Caspase-3活性升高。依达拉奉可以提高细胞增殖能力,降低MDA含量,降低ROS水平,增强SOD活性,减少细胞凋亡,下调Bax蛋白和 mRNA表达,上调Bcl-2蛋白和mRNA表达,降低Caspase-3活性(P<0.05)。结论依达拉奉通过减轻氧化应激和抑制细胞凋亡而减轻顺铂诱导的大鼠肾小管上皮细胞损伤。
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