Objective To explore the effects of iguratimod on cell proliferation and apoptosis of human multiple myeloma cell line RPMI8226 cells. Methods The experiment was divided into control group (0 μg/ml iguratimod), 10 μg/ml iguratimod group, 20 g/ml iguratimod group, and 30 μg/ml iguratimod group. After treated RPMI8226 cells with different concentrations of iguratimod for 24 h, the cell viability was measured using MTT assay, the morphology of apoptotic cell was observed under a fluorescence microscope after Hoechst 33258 staining, the expression level of Notch1 m RNA was detected by quantitative real-time PCR, and the expression levels of Bax and Notch1 protein were detected by Western blot. Results Compared with control group, iguratimod significantly reduced the viability of RPMI8226 cells in a dose dependent manner (P ＜ 0. 05). The cell nuclei showed pyknosis and lysis in RPMI8226 cells treated with iguratimod (10, 20, and 30 μg/ml) for 24 h, and the expression level of Bax protein was upregulated (P ＜ 0. 05). In addition, the levels of Notch1 m RNA as well as protein in RPMI8226 cells were markedly ameliorated after treatment with iguratimod (10, 20, and 30 μg/ml) for 24 h (P ＜ 0. 05). Conclusion Iguratimod can inhibit cell proliferation and induce cell apoptosis of human myeloma cell line RPMI8226, which may be related to inhibition of Notch pathway activation.%目的 探讨艾拉莫德对人多发性骨髓瘤 (multiple myeloma, MM) RPMI8226细胞增殖和凋亡的影响.方法 实验分组为:对照组 (0μg/ml艾拉莫德), 10μg/ml艾拉莫德处理组, 20μg/ml艾拉莫德处理组, 30μg/ml艾拉莫德处理组.艾拉莫德 (10, 20, 30μg/ml) 作用于人多发性骨髓瘤细胞株RPMI8226细胞24 h, 采用MTT法检测RPMI8226细胞活力, Hoechst 33258染色检测凋亡细胞;荧光定量PCR检测Notch1 m RNA表达水平; Western blot检测Bax和Notch1蛋白的表达水平.结果10, 20和30μg/ml的艾拉莫德处理24 h, 可降低RPMI8226细胞活力, 并具剂量依赖性 (P ＜0. 05) .艾拉莫德 (10, 20, 30μg/ml) 处理RPMI8226细胞24 h, 细胞核出现固缩、裂解现象.10, 20和30μg/ml的艾拉莫德处理细胞24 h可显著上调RPMI8226细胞的Bax蛋白表达水平 (P ＜0. 05), 并显著下调Notch1 m RNA和蛋白水平 (P ＜0. 05) .结论 艾拉莫德可抑制人多发性骨髓瘤细胞株RPMI8226细胞增殖并促进细胞凋亡, 其作用机制可能与其抑制Notch通路的活化有关.
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