肿瘤药学
腫瘤藥學
종류약학
ANTI-TUMOR PHARMACY
2013年
1期
22-25
,共4页
卵巢癌%8-溴-7-甲氧基白杨素%凋亡%Bim
卵巢癌%8-溴-7-甲氧基白楊素%凋亡%Bim
란소암%8-추-7-갑양기백양소%조망%Bim
Ovarian cancer%BrMC%Apoptosis%Bim
目的探讨8-溴-7-甲氧基白杨素(8-bromo-7-methoxychrysin, BrMC)诱导人卵巢癌A2780细胞凋亡的作用及其可能机制.方法采用不同浓度(2.5、5.0和10.0μmol·L-1)的BrMC处理体外培养的A2780细胞,通过碘化丙啶(PI)染色流式细胞术(FCM)和ELISA法检测细胞凋亡的情况,Western Blot检测Bim和caspase-3蛋白的表达水平.结果不同浓度(2.5、5.0和10.0μmol·L-1)BrMC均可促进A2780细胞的凋亡,且细胞凋亡率随BrMC浓度的升高而上升.不同浓度(5.0和10.0μmol·L-1)BrMC作用的A2780细胞中Bim蛋白的表达均较正常对照组显著增加,而通过siRNA干扰下调Bim蛋白的表达能显著抑制BrMC诱导的A2780细胞凋亡.结论 BrMC可诱导人卵巢癌A2780细胞凋亡,促进Bim蛋白的表达可能是其作用机制之一.
目的探討8-溴-7-甲氧基白楊素(8-bromo-7-methoxychrysin, BrMC)誘導人卵巢癌A2780細胞凋亡的作用及其可能機製.方法採用不同濃度(2.5、5.0和10.0μmol·L-1)的BrMC處理體外培養的A2780細胞,通過碘化丙啶(PI)染色流式細胞術(FCM)和ELISA法檢測細胞凋亡的情況,Western Blot檢測Bim和caspase-3蛋白的錶達水平.結果不同濃度(2.5、5.0和10.0μmol·L-1)BrMC均可促進A2780細胞的凋亡,且細胞凋亡率隨BrMC濃度的升高而上升.不同濃度(5.0和10.0μmol·L-1)BrMC作用的A2780細胞中Bim蛋白的錶達均較正常對照組顯著增加,而通過siRNA榦擾下調Bim蛋白的錶達能顯著抑製BrMC誘導的A2780細胞凋亡.結論 BrMC可誘導人卵巢癌A2780細胞凋亡,促進Bim蛋白的錶達可能是其作用機製之一.
목적탐토8-추-7-갑양기백양소(8-bromo-7-methoxychrysin, BrMC)유도인란소암A2780세포조망적작용급기가능궤제.방법채용불동농도(2.5、5.0화10.0μmol·L-1)적BrMC처리체외배양적A2780세포,통과전화병정(PI)염색류식세포술(FCM)화ELISA법검측세포조망적정황,Western Blot검측Bim화caspase-3단백적표체수평.결과불동농도(2.5、5.0화10.0μmol·L-1)BrMC균가촉진A2780세포적조망,차세포조망솔수BrMC농도적승고이상승.불동농도(5.0화10.0μmol·L-1)BrMC작용적A2780세포중Bim단백적표체균교정상대조조현저증가,이통과siRNA간우하조Bim단백적표체능현저억제BrMC유도적A2780세포조망.결론 BrMC가유도인란소암A2780세포조망,촉진Bim단백적표체가능시기작용궤제지일.
ABSTRACT:Objective To investigate the effects of 8-bromo-7-methoxychrysin (BrMC) on the apoptosis in human ovarian cancer cells and its possible mechanisms. Methods Human ovarian cancer A2780 cells were cultured in vitro and treated with different concentrations (2.5, 5.0, 10.0μmol·L-1) of BrMC and 50μmol·L-1 chrysin. The apoptosis were evaluated by flow cytometry (FCM) after propidium iodide (PI) staining and enzyme-linked immunosorbent assay (ELISA). The expressions of Bim and caspase-3 protein were analyzed by Western Blot. Results Different concentrations(2.5, 5.0, 10.0μmol·L-1) of BrMC significantly increased the apoptotic rates in A2780 cells in a concentration dependent manner. Furthermore, different concen-trations (5.0, 10.0μmol·L-1) of BrMC efficaciously up-regulated the Bim expression. But down-regulation of Bim by siRNA significantly inhibited the apoptosis and caspase-3 cleavage in A2780 cells induced by BrMC. Conclusion BrMC could obviously induce the apoptosis in human ovarian cancer A2780 cells, and up-regulation of Bim expression may be involved in this process.