褐藻多糖对乳腺癌细胞活性的影响及机制探讨

摘要

目的：观察褐藻多糖对人乳腺癌细胞株MCF-7、MDA-MB-231细胞活性的影响，并探讨其作用机制。方法将对数生长期的MCF-7、MDA-MB-231细胞（观察A组、B组）分别加入100、200μg／mL褐藻多糖2 mL，对照A组、B组均加入等体积的DMEM培养基2 mL。用台盼蓝染色实验测算细胞增殖抑制率，用流式细胞仪检测细胞周期和凋亡细胞，用Western blot法检测细胞Caspase-8及磷酸化细胞外调节蛋白激酶（ p-Erk ）、Erk表达。结果随着褐藻多糖浓度增加、作用时间延长，观察A组、B组细胞增殖抑制率逐渐升高（P均＜0．05）；观察A组、B组G0／G1期细胞比例升高、S期及G2期细胞比例降低，细胞凋亡率增高，褐藻多糖浓度高者变化更明显，P均＜0．05；观察A组、B组细胞Caspase-8表达升高、p-Erk表达下降，褐藻多糖浓度高者变化更明显，P均＜0．05。结论褐藻多糖可抑制MCF-7、MDA-MB-231细胞增殖，阻滞细胞周期于G0／G1期，促进细胞凋亡；该作用可能是通过上调细胞Caspase-8表达、下调p-Erk表达水平实现。%Objective To observe the effects of Fucoidan on cell viability of breast cancer cell lines MCF -7 and MDA-MB-231 and to investigate its possible mechanism .Methods The breast cancer cell lines MCF-7 and MDA-MB-231 in the logarithmic phase ( observation group A and B ) were respectively treated with 2 mL Fucoidan ( 100 ug/mL and 200 ug/mL) .The control group A and B were treated with the same volume of DMEM culture medium .The cell proliferation inhi-bition rate was detected by Trypan blue staining , cell cycle and apoptosis cells were analyzed by flow cytometry , and the expression of Caspase-8, phosphorylation Erk ( p-Erk) and total Erk was detected by Western blotting .Results With the increased Fucoidan concentration and the prolonged time , the cell proliferation inhibition rates of the observation groups A and B were increased (all P<0.05), the cell proportion in the G0/G1 phase of the observation groups A and group B was increased, the cell proportion in the S phase and G2 was reduced, the apoptosis rate was increased, and the changes in the high concentration Fucoidan group were more significant (all P<0.05).The expression of Caspase-8 was increased and the Erk expression was decreased in the observation groups A and B , and the changes in the high concentration Fucoidan group were more significant (all P<0.05).Conclusion Fucoidan could inhibit the proliferation of MCF-7 and MDA-MB-231 cell lines, arrest the breast cells in G0/G1 phase, and also promote the apoptosis.This mechanism may be achieved by activating the expression of Caspase-8 and down-regulating the p-Erk expression .