目的探讨Nur77特异性激动剂Csn-B联合伊马替尼通过促进Nur77表达而发挥的抗慢性粒细胞白血病（CML）活性，并探讨其信号通路的潜在作用。首先采用CCK-8和Transwell实验检测Csn-B、伊马替尼及其组合对K562细胞增殖和迁移的抑制作用。流式细胞仪检测Csn-B、伊马替尼及其联合处理后K562细胞的凋亡率。 Western blot检测K562细胞中Nur77、Pim-1、Drp1、p-Drp1 S616、Bcl-2、Bax的表达水平。最后采用免疫荧光法检测Csn-B、伊马替尼及其组合处理后的K562细胞中活性氧（ROS）的表达水平。GSE43754数据集中，CML患者中Nur77的水平较正常人群显着降低（P < 0.001）。 Csn-B联合伊马替尼可显着抑制K562细胞的增殖和迁移（均P < 0.001），并诱导细胞凋亡（P < 0.001）。 Csn-B 促进 K562 细胞中 Nur77 的表达，与伊马替尼联合使用可协同增强伊马替尼敏感性。与单药治疗相比，Csn-B联合伊马替尼可显着增强K562细胞和线粒体中ROS水平（均P < 0.001）。Csn-B联合伊马替尼可增强ROS表达，通过Nur77/Pim-诱导K562细胞凋亡。 1/Drp1 途径。

To investigate the anti- chronic myelogenous leukemia (CML) activity of Nur77-specific agonist Csn-B combined with imatinib by promoting Nur77 expression, and explore the potential role of its signaling pathway.Firstly, CCK-8 and Transwell assay were used to detect the inhibitory effects of Csn-B, imatinib, and their combination on the proliferation and migration of K562 cells. Furthermore, the apoptosis rate of K562 cells treated with Csn-B, imatinib, and their combination was detected by flow cytometry. The expression levels of Nur77, Pim-1, Drp1, p-Drp1 S616, Bcl-2 and Bax in K562 cells were detected by Western blot. Finally, the expression levels of reactive oxygen species (ROS) in K562 cells treated with Csn-B, imatinib and their combination were detected by immunofluorescence assay.The level of Nur77 in CML patients decreased significantly compared with normal population in dataset of GSE43754 (P < 0.001). Csn-B combined with imatinib could significantly inhibit the proliferation and migration of K562 cells (both P < 0.001), and induce apoptosis (P < 0.001). Csn-B promoted Nur77 expression in K562 cells, and synergistically enhanced imatinib sensitivity when combined with imatinib. Csn-B combined with imatinib could significantly enhanced ROS levels in K562 cells and mitochondria compared with single-drug treatment (both P < 0.001).Csn-B combined with imatinib can enhance ROS expression and induce apoptosis of K562 cells through Nur77/Pim-1/Drp1 pathway.