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目的：探讨去甲斑蝥素抗肿瘤作用的分子机制。方法：用 10μ g/ml去甲斑蝥素处理体外培养的人乳腺癌细胞系 MCF-7。处理后，在不同时间点，采用普通光镜、电子显微镜观察去甲斑蝥素对乳腺癌细胞的诱导凋亡现象。利用流式细胞仪分析凋亡细胞百分比，用蛋白印迹杂交方法对凋亡抑制基因 bcl-2的表达情况进行检测。结果：经 10μ g/ml去甲斑蝥素处理 12 h后，可观察到 MCF-7细胞变形、出泡，从培养瓶底脱离。细胞染色和电子显微镜可观察到染色质浓聚、边集，且随着药物作用时间的延长，凋亡细胞百分比逐渐增加。与对照组相比，凋亡抑制基因 bcl-2的表达降低。结论 :诱导肿瘤细胞凋亡可能是去甲斑蝥素抗肿瘤作用的分子机制之一。
Objective: To explore the molecular mechanism of anticancer effect of norcantharidin. METHODS: In vitro cultured human breast cancer cell line MCF-7 was treated with 10 μg/ml norcantharidin. After treatment, ordinary light microscope and electron microscope were used to observe the apoptosis-inducing effect of norcantharidin on breast cancer cells at different time points. The percentage of apoptotic cells was analyzed by flow cytometry, and the expression of apoptosis-suppressing gene bcl-2 was detected by Western blotting. RESULTS: After treatment with 10 μg/ml norcantharidin for 12 h, MCF-7 cells were observed to be deformed and blebbed and detached from the bottom of the culture flask. Chromatin concentration and edge collection were observed by cell staining and electron microscopy, and the percentage of apoptotic cells gradually increased with the prolongation of drug action. Compared with the control group, the expression of apoptosis suppressor gene bcl-2 was decreased. Conclusion : Inducing apoptosis of tumor cells may be one of the molecular mechanisms of anticancer effect of norcantharidin.