摘要
目的:研究二烯丙基二硫(DADS)诱导人乳腺癌MCF-7细胞凋亡及其分子机制。方法:AO／EB荧光染色法、流式细胞仪检测细胞凋亡率;Western blot法检测DADS对caspase-3剪切片断的影响,及对MAPKs通路相关蛋白,包括p-JNK、JNK表达的影响。结果:DADS对乳腺癌细胞株MCF-7生长具有明显的抑制作用,经AO／EB形态变化分析,可见明显的细胞凋亡特征;DADS处理MCF-7细胞6、12、24、48 h,流式细胞仪检测细胞的凋亡率分别为3．74％、9．22％、20.2％、42％,而对照组细胞的凋亡率仅为3．03％(P<0．05);不同浓度的DADS作用于MCF-7细胞24 h后,Western blot法检测发现caspase-3出现断裂片断,并随着浓度的增加断裂更明显。进一步研究发现,DADS处理MCF-7细胞后,JNK磷酸化水平明显升高。结论:DADS能诱导乳腺癌细胞株MCF-7细胞凋亡,JNK信号通路抑制可能是DADS诱导其调亡的分子机制之一。
Aim To study the effect of DADS in induction of apoptosis in human breast cancer MCF-7 cells and its mechanisms. Methods： Apoptofic cells were examined using AO/EB. fluorescent staining and flow cytometry. Protein expression was detected by Western blot analysis. Results： DADS inhibited proliferation of MCF-7 cells. AO/EB fluorescent showed series of apoptotic changes in MCF-7 cells. Flow cytometry indicated that apoptofic ratio increased rapidly for 200μmol·L^-1 DADS. Cleavage at the caspase-3 was observed in MCF-7 cells after treatment with different doses of DADS for 24 h. After MCF-7 cells were treated with 200μmol·L^-1 of DADS for different times, Western Blot analysis showed stress-actived protein kinase （SAPK/ JNK） mitogen-actived proteinn kinase were activated obviously afer 6 h. Conclusions： DADS inhibited proliferation of MCF-7 cells and induced apoptosis of MCF-7 cells. Activation of SAPK/JNK pathway may be one of its mechanisms.
出处
《现代生物医学进展》
CAS
2007年第3期344-346,共3页
Progress in Modern Biomedicine
基金
国家自然科学基金项目(N030300426)
湖南省教育厅青年基金(No03B034)
