AIM:ToexploretheeffectofcelastrolonapoptosisofSaos-2cellsanditsmechanism.METH-ODS:Saos-2 cells were treated with various concentrations of celastrol , and the cell viability was measured by MTT assay . Apoptosis and reactive oxygen species ( ROS) production were determined by flow cytometry .The protein levels of cleaved caspase-9, cleaved caspase-3 and phosphorylated JNK were evaluated by Western blot .RESULTS:The viability of Saos-2 cells was significantly inhibited by celastrol .Celastrol significantly induced apoptosis of Saos-2 cells.Celastrol signifi-cantly induced ROS production in the Saos-2 cells.Western blot analysis demonstrated that celastrol significantly increased the protein levels of cleaved caspase-9, cleaved caspase-3 and phosphorylated JNK in the Saos-2 cells.CONCLUSION:Celastrol induces caspase-dependent apoptosis through ROS/JNK pathway in Saos-2 cells.%目的：探讨雷公藤红素对人骨肉瘤细胞Saos－2的杀伤作用及相关机制。方法：将人骨肉瘤细胞Saos－2用各种不同的浓度的雷公藤红素治疗后，采用MTT法检测雷公藤红素对Saos－2细胞活力的抑制作用；采用流式细胞术检测用雷公藤红素处理后Saos－2细胞的凋亡及活性氧簇（ ROS）的产生；Western blot检测雷公藤红素处理后Saos－2细胞cleaved caspase－9、cleaved caspase－3和磷酸化JNK的表达水平。结果：雷公藤红素有显著的体外抗骨肉瘤作用，能显著抑制Saos－2细胞的活力。雷公藤红素可显著诱导Saos－2细胞发生凋亡，产生ROS。雷公藤红素处理后Saos－2细胞cleaved caspase－9、cleaved caspase－3和磷酸化JNK的表达水平均显著上升。结论：雷公藤红素通过ROS／JNK途径诱导人骨肉瘤Saos－2细胞发生caspase依赖的凋亡。
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