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目的研究百合多糖1(LP1)对二甲双胍的抗乳腺癌细胞作用的影响。方法培养MCF-7乳腺癌细胞,加入(0.5、1.0)mg/m L LP1和(5、10、20、50)mmol/L的二甲双胍,MTT法检测LP1和二甲双胍对MCF-7细胞增殖的影响;异硫氰酸荧光素标记的膜联素Ⅴ/碘化丙啶(annexinⅤ-FITC/PI)双染色结合流式细胞术观察细胞周期和细胞凋亡;Western blot法检测Bcl-2、Bax、腺苷酸活化蛋白激酶(AMPK)和磷酸化腺苷酸活化蛋白激酶(p-AMPK)蛋白含量。结果 1 mg/m L LP1可以增强二甲双胍的抗增殖作用、细胞周期阻滞于G1期作用和诱导细胞凋亡作用。LP1处理增强二甲双胍对Bcl-2蛋白的下调和Bax蛋白的上调作用,但不影响二甲双胍对MAPK通路的激活作用。结论 LP1增强二甲双胍对MCF-7乳腺癌细胞的抗增殖作用,促进细胞凋亡,其机制与凋亡蛋白Bcl-2和Bax参与有关。
Objective To investigate the effect of lily polysaccharide 1 (LP1) on the anti-breast cancer cell effect of metformin. Methods MCF-7 breast cancer cells were cultured and cultured with (0.5,1.0) mg / mL LP1 and (5,10,20,50) mmol / L metformin. The effects of LP1 and metformin on the proliferation of MCF-7 cells were detected by MTT assay ; Cell cycle and apoptosis were observed by double-staining with fluorescein isothiocyanate labeled annexinⅤ-FITC / PI; Bcl-2, Bax, Adenosine Activated Protein Kinase (AMPK) and Phosphorylated Adenylate Activated Protein Kinase (p-AMPK) Protein Content. Results LP1 1 mg / m L could enhance the anti-proliferative effect of metformin, arrest the cell cycle in G1 phase and induce apoptosis. LP1 treatment enhanced the down-regulation of Bcl-2 protein and up-regulation of Bax protein by metformin, but did not affect the activation of MAPK pathway by metformin. Conclusion LP1 can enhance the antiproliferative effect of metformin on MCF-7 breast cancer cells and promote apoptosis. The mechanism is related to the involvement of apoptosis proteins Bcl-2 and Bax.