山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2015年
30期
5-7
,共3页
褐藻多糖%乳腺癌%细胞周期%细胞凋亡%半胱氨酸天冬氨酸蛋白酶8%细胞外调节蛋白激酶
褐藻多糖%乳腺癌%細胞週期%細胞凋亡%半胱氨痠天鼕氨痠蛋白酶8%細胞外調節蛋白激酶
갈조다당%유선암%세포주기%세포조망%반광안산천동안산단백매8%세포외조절단백격매
Fucoidan,breast carcinoma%cell cycle%apoptosis%caspase%extracellular signal-regulated kinases
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。
目的:觀察褐藻多糖對人乳腺癌細胞株MCF-7、MDA-MB-231細胞活性的影響,併探討其作用機製。方法將對數生長期的MCF-7、MDA-MB-231細胞(觀察A組、B組)分彆加入100、200μg/mL褐藻多糖2 mL,對照A組、B組均加入等體積的DMEM培養基2 mL。用檯盼藍染色實驗測算細胞增殖抑製率,用流式細胞儀檢測細胞週期和凋亡細胞,用Western blot法檢測細胞Caspase-8及燐痠化細胞外調節蛋白激酶( p-Erk )、Erk錶達。結果隨著褐藻多糖濃度增加、作用時間延長,觀察A組、B組細胞增殖抑製率逐漸升高(P均<0.05);觀察A組、B組G0/G1期細胞比例升高、S期及G2期細胞比例降低,細胞凋亡率增高,褐藻多糖濃度高者變化更明顯,P均<0.05;觀察A組、B組細胞Caspase-8錶達升高、p-Erk錶達下降,褐藻多糖濃度高者變化更明顯,P均<0.05。結論褐藻多糖可抑製MCF-7、MDA-MB-231細胞增殖,阻滯細胞週期于G0/G1期,促進細胞凋亡;該作用可能是通過上調細胞Caspase-8錶達、下調p-Erk錶達水平實現。
목적:관찰갈조다당대인유선암세포주MCF-7、MDA-MB-231세포활성적영향,병탐토기작용궤제。방법장대수생장기적MCF-7、MDA-MB-231세포(관찰A조、B조)분별가입100、200μg/mL갈조다당2 mL,대조A조、B조균가입등체적적DMEM배양기2 mL。용태반람염색실험측산세포증식억제솔,용류식세포의검측세포주기화조망세포,용Western blot법검측세포Caspase-8급린산화세포외조절단백격매( p-Erk )、Erk표체。결과수착갈조다당농도증가、작용시간연장,관찰A조、B조세포증식억제솔축점승고(P균<0.05);관찰A조、B조G0/G1기세포비례승고、S기급G2기세포비례강저,세포조망솔증고,갈조다당농도고자변화경명현,P균<0.05;관찰A조、B조세포Caspase-8표체승고、p-Erk표체하강,갈조다당농도고자변화경명현,P균<0.05。결론갈조다당가억제MCF-7、MDA-MB-231세포증식,조체세포주기우G0/G1기,촉진세포조망;해작용가능시통과상조세포Caspase-8표체、하조p-Erk표체수평실현。
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 .