目的：探讨1, 25-二羟维生素D（VD3）对人乳腺癌MCF-7细胞凋亡的影响及其作用机制。方法：取体外培养的人乳腺癌MCF-7 细胞，随机分为6 组：对照组、2-脱氧葡萄糖（2-DG，葡萄糖抑制剂）组、1 μmol/L VD3组、10 μmol/L VD3组、2-DG+1 μmol/L VD3组和2-DG+10 μmol/L VD3组。药物干预6组细胞48 h后，以葡萄糖摄取测定试剂盒检测细胞的葡萄糖摄取量、ATP试剂盒检测细胞中ATP含量和乳酸试剂盒检测细胞的乳酸水平，WB法检测MCF-7细胞中细胞色素C（Cyt c）和凋亡相关蛋白（Bcl-2、BAX、 PARP1、caspase9和caspase3）的表达水平。结果：与对照组比较，VD3 干预后，MCF-7细胞的凋亡率明显增加（P<0.05或P<0.01），同时细胞的葡萄糖摄取量、ATP含量及乳酸水平均明显降低（P<0.05 或P<0.01），Cyt c、BAX、PARP1、caspase9 及caspase3蛋白表达量明显升高（均P<0.05），Bcl-2蛋白表达量降低（P<0.05或P<0.01）；VD3联合2-DG干预后，各组细胞检测指标的变化更为明显（P<0.05或P<0.01）。结论：VD3可通过抑制人乳腺癌MCF-7细胞的糖酵解过程并以线粒体的Cyt c途径促进细胞凋亡。

Objective: To investigate the effect of 1, 25-dihydroxyvitamin D3 (VD3) on apoptosis of human breast cancer MCF-7 cells and its mechanism. Methods: Human breast cancer MCF-7 cells cultured in vitro were randomly divided into 6 groups: control group, 2-DG group, 1 μmol/L VD3 group, 10 μmol/L VD3 group, 2-DG+1 μmol/L VD3 group and 2-DG+10 μmol/L VD3 group. The cells in 6 groups were detected 48 h after they were treated with VD3 or 2-DG. The glucose uptake assay was used to measure the glucose uptake of cells, the ATP content in the cells was measured by the ATP kit, and the lactate level was measured by the lactate kit. The expression levels of cytochrome C (Cyt c) and apoptosis-associated proteins (Bcl-2, BAX, PARP1, caspase9 and caspase3) in MCF-7 cells were detected by WB method. Results: Compared with the control group, after the intervention of VD3, the apoptosis rate of MCF-7 cells increased significantly (P<0.05 or P<0.01), the glucose uptake, ATP content and lactate level were significantly decreased (P<0.05 or P<0.01), the expression of Cyt c, BAX, PARP1, caspase9 and caspase3 protein was significantly increased (all P<0.05), and the expression of Bcl-2 protein was decreased (P<0.05 or P<0.01); after the intervention of VD3 combined with 2-DG, the changes in the detection indexes of each group were more obvious (P<0.05 or P<0.01). Conclusion: VD3 can inhibit glycolysis of human breast cancer MCF-7 cells and induce apoptosis through the mitochondrial Cyt c pathway.

武汉市卫生健康委员会科研基金（No.WX19D33）