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目的：探讨多西他赛固体脂质纳米粒抗乳腺癌效果及机制研究。方法：本实验采用MTT 法考察了多西他赛固体脂质纳米粒对人乳腺癌MCF-7 细胞增殖的抑制作用，采用流式细胞术检测多西他赛固体脂质纳米粒对MCF-7 肿瘤细胞凋亡作用，并进一步应用Western-Blot 印迹法观察多西他赛固体脂质纳米粒对MCF-7 细胞中Src、E-cadherin、β-catenin蛋白表达的影响，探索了其抗乳腺肿瘤的作用机制。结果：多西他赛固体脂质纳米粒能够显著抑制人乳腺癌MCF-7 肿瘤细胞的增殖，且浓度越高，抑制率越大（P<0.05）。经25、50、100 滋g/mL 多西他赛固体脂质纳米粒制剂作用24 h后，人乳腺癌细胞MCF-7 的凋亡率分别为14.56%、 21.21%、29.94%，细胞凋亡率随着药物浓度的增加而增加，且各实验组间比较有显著性差异（P<0.05）。人乳腺癌MCF-7 肿瘤细胞经不同浓度的多西他赛固体脂质纳米粒处理后，细胞中E-cadherin 蛋白表达显著升高，Src、β-catenin 蛋白表达显著降低，且呈现出明显的剂量依赖性。结论：多西他赛固体脂质纳米粒能够抑制人乳腺癌MCF-7 细胞增殖，促进其凋亡，可能与下调β-catenin 蛋白的表达，上调E-cadherin 蛋白表达以及抑制Src激酶活性有关。

英文摘要:

Objective:To investigate the antitumor effect and the mechanism of docetaxel loaded solid lipid nanoparticles on breast cancer cells.Methods:Inhibitory effect of docetaxel loaded solid lipid nanoparticles on the proliferation of human breast cancer cell line MCF-7 was tested by MTT method, apoptosis of tumor cells was detected by flow cytometry, the expression of Src, E-cadherin and β-Catenin protein inMCF-7 cells cultured with docetaxel loaded solid lipid nanoparticles were tested byWestern-Blot method.Results:Docetaxel loaded solid lipid nanoparticles had strong inhibition on the proliferation of human breast cancer MCF-7 tumor cells. After incubation with 25, 50, 100 滋g/ml of docetaxel solid lipid nanoparticle preparation for 24 h, human breast cancer MCF-7 cell line showed different apoptosis rates of 14.56%, 21.21%, 29.94%, cell apoptosis increased with drug concentration and there was a significant difference between any two experimental groups (P<0.05). The Src, E-cadherin and β-Catenin protein expression in MCF-7 cells treated with different concentrations of docetaxel loaded solid lipid nanoparticles showed a significant dose dependent effect. As the drug concentration increased, the E-cadherin protein expression level also rose significantly, but the Src and β-catenin protein expression levels dropped significantly.Conclusion:Docetaxel loaded solid lipid nanoparticles can inhibit the proliferation of breast cancer cells. The mechanism may be related to up-regulation of the expression of E-cadherin protein, down-regulation of the expression of β-catenin pro- tein, and the inhibition of Src kinase activity.

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