摘要
目的:研究褐藻糖胶(fucoidan)对体外培养的人乳腺癌MCF-7细胞增殖及凋亡的影响,并探讨其凋亡机制。方法:应用MTT法检测细胞的增殖;Hoechst33258染色、琼脂糖凝胶电泳法观察细胞的凋亡;RT-PCR和Western印迹法分别检测细胞中bcl-2和bax的mRNA及其蛋白的表达。结果:不同浓度的褐藻糖胶均能抑制MCF-7细胞的增殖(P<0.01),并随其浓度增加,抑制率逐渐增大;褐藻糖胶诱导MCF-7细胞凋亡数增加,且可见明显的、凋亡特有的DNA梯形条带;在褐藻糖胶存在下,bcl-2基因的mRNA和蛋白表达减少,bax基因的mRNA和蛋白表达增加,bcl-2/bax比值下降(P<0.05)。结论:褐藻糖胶可抑制MCF-7细胞增殖,且诱导其凋亡,其凋亡机制可能与下调bcl-2和上调bax基因的表达有关。
Objective： To investigate the effects of fucoidan on proliferation and apoptosis of breast carcinoma cell line MCF-7 and the underlying mechanism. Methods ：Cell viability was measured by MTT assay. Apoptosis was detected by Hoechst 33258 staining and agarose gel electrophoresis. The mRNA and protein expression of bcl-2 and bax were examined by RT-PCR and Western blotting, respectively. Results： Fucoidan effectively inhibited the proliferation of MCF-7 cells in a concentration-dependent manner （P 〈 0. O1 ）. Fucoidan induced significant apoptosis of MCF-7 cells characterized by fragmented DNA ladder. Fucoidan down-regulated the expression of bcl-2 and up-regulated bax at mRNA and protein levels. The ratio of bcl-2 to bax decreased with the increase in the fucoidan concentrations （ P 〈 0. 05 ）. Conclusion. Fucoidan inhibites the proliferation and induced the apoptosis of MCF-7 cells. The underlying mechanism may be related with down-regulation of anti-apoptotic protein bcl-2 and up-regulation of apoptotic protein bax.
出处
《肿瘤》
CAS
CSCD
北大核心
2008年第3期220-223,共4页
Tumor
基金
青岛市科技局科技计划资助项目(编号:03-1-YN-14)
