目的   探讨二肽基肽酶-4（DPP-4）抑制剂阿拉格列汀（anagliptin）抑制结直肠癌肺转移瘤的作用机制。 方法   24只雄性BALB/c小鼠随机分为对照组、模型组和anagliptin组。对照组不进行任何处理，模型组于小鼠尾静脉一次性注射浓度为1×109/L的CT-26细胞溶液0.1ml后构建肺转移瘤模型，anagliptin组构建肺转移瘤模型0 d后腹腔注射anagliptin 20 mg/(kg·d)，14 d后处死实验动物。通过HE染色观察小鼠肺部形态结构。通过MTT实验测定CT-26细胞活力，流式细胞术及活死细胞染色检测CT-26细胞凋亡。活性氧试剂盒测定细胞活性氧簇（ROS）生成，Western blotting测定Bcl-2、Bax，cleaved-Caspase-3、超氧化物歧化酶（SOD）-1和SOD-2表达。 结果  观察到给予anagliptin后可明显抑制模型组肺组织结构的异常改变。Anagliptin浓度为2 mmol/L时抑制CT-26细胞活力，anagliptin具有促CT-26细胞凋亡的作用，CT-26细胞孵育anagliptin后发现细胞内ROS生成增加。蛋白水平检测发现，CT-26细胞孵育anagliptin后Bax和cleaved-Caspase-3表达升高，而Bcl-2表达下降，给予anagliptin后抑制CT-26细胞SOD-1表达，而对SOD-2无影响。 结论   Anagliptin通过SOD-1/ROS途径促结直肠癌细胞凋亡，抑制肺转移瘤的形成。 

Objective  To investigate the formation and mechanism of dipeptidylpeptidase-4 inhibitor anagliptin inhibiting lung metastasis of colorectal cancer.  Methods   Twenty-four male BALB/c mice were randomly divided into normal group, model group, anagliptin group. The control group did not undergo any treatment. The model group was injected with 0.1 ml CT-26 cells of 109 cells/L. once through the tail vein of the mouse to construct a lung metastasis model, while the anagliptin group was injected intraperitoneally 20mg/(kg·d) 0 day after  constructing a lung metastasis model. The mice were sacrificed after 14 days. HE staining was used to detect the morphological alteration. Determination of CT-26 cell viability through MTT assay and CT-26 cell apoptosis was detected by flow cytometry and live/dead cell staining. Reactive oxygen species(ROS) production was measured by ROS kit. Western blotting was conducted to measure the expression level of Bcl-2, Bax, cleaved-caspase-3, superoxide dismutase(SOD-1) and SOD-2.  Results   HE staining showed that the administration of anagliptin could significantly inhibit the abnormal changes in the model group. Anagliptin inhibited the viability of CT-26 cells above 2 mmol/L. Anagliptin promoted the apoptosis of CT-26 cells. Incubation of anagliptin in CT-26 cells significant promoted the production of ROS. Incubation of anagliptin stimulated the expressions of Bax and cleaved-Caspase-3, while down-regulated the expression of Bcl-2 in CT-26 cells. Administration of anagliptin decreased the expression of SOD-1, but not SOD-2.  Conclusion   Anagliptin promotes apoptosis of colorectal cancer cells and inhibits the formation of lung metastatic tumors through the SOD-1/ROS pathway.