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目的研究desmosdumotin-C(Des-C)B环对位氟修饰衍生物TPP对人乳腺癌细胞MCF-7的增殖抑制作用,并探讨其作用机制。方法 MTT法检测质量浓度为1.0、2.5、5.0、10.0、20.0μg/m L的TPP作用48 h后,对MCF-7细胞的增殖抑制率;流式细胞术检测20.0μg/m L TPP作用0、24、48 h诱导MCF-7细胞的凋亡程度;流式细胞术检测20.0μg/m L TPP作用0、24、48 h对MCF-7细胞中NF-κB P65阳性细胞表达率的影响。结果作用48 h后,2.5、5.0、10.0、20.0μg/m L的TPP对MCF-7细胞增殖均有显著抑制作用,且抑制率随着浓度的升高而增大;20μg/m L TPP作用24、48 h均可诱导细胞凋亡;作用48 h后,20μg/m L TPP可显著减少MCF-7中NF-κB P65阳性细胞率。结论 TPP显著抑制MCF-7细胞增殖,诱导MCF-7细胞凋亡,作用机制可能与下调NF-κB表达有关。
Objective To study the inhibitory effect of TPM, a fluorinated derivative of B-cyclic desmosdumotin-C (Des-C), on the proliferation of human breast cancer cell line MCF-7 and to explore its mechanism. Methods MTT method was used to detect the proliferation of MCF-7 cells treated with 1.0, 2.5, 5.0, 10.0 and 20.0 μg / ml of TPP for 48 h. Flow cytometry was used to detect the effect of TPP 20.0 μg / m L , 24,48 h, respectively. The effect of 20.0 μg / ml TPP on the expression of NF-κB P65 positive cells in MCF-7 cells was detected by flow cytometry. Results After 48 h treatment, 2.5, 5.0, 10.0 and 20.0 μg / ml of TPP significantly inhibited the proliferation of MCF-7 cells, and the inhibition rate increased with the increase of concentration. TPP effect of 20 μg / ml Twenty-four hours and forty-eight hours, the apoptosis of MCF-7 cells was induced by TPP at a dosage of 20 μg / ml for 48 h. Conclusion TPP can significantly inhibit the proliferation of MCF-7 cells and induce the apoptosis of MCF-7 cells. The mechanism may be related to the down-regulation of NF-κB expression.