CAJ | 학술논문

目的：探讨黄芩苷和黄芩素联合应用对乳腺癌细胞凋亡的诱导作用及其相关机制。方法将不同浓度的黄芩苷、黄芩素以及两者联合作用于人乳腺癌(Michigan Cancer Foundation 7，MCF-7)细胞。检测上述化合物对乳腺癌细胞的活力、凋亡情况以及凋亡相关蛋白表达的影响。结果黄芩苷或黄芩素作用于乳腺癌细胞后，与作用前相比细胞生长抑制率显著升高(P<0.05)；两者联合应用，与两者单独作用相比抗增殖作用明显增强(P<0.05)。流式细胞术检测发现两者作用后尤其是两者联用后细胞凋亡显著增加。蛋白印迹分析显示黄芩苷和黄芩素联合作用后Caspase-3、Caspase-9、Bax和p53的表达增加而Bcl-2表达下降，同时p-38活化亦增加。结论黄芩苷和黄芩素均能诱导乳腺癌细胞的凋亡，两者联合应用后作用明显增强，其机制可能与其促进促凋亡相关蛋白Caspase-3、Caspase-9、Bax和p53等的表达，并抑制抗凋亡蛋白Bcl-2的表达有关。
목적：탐토황금감화황금소연합응용대유선암세포조망적유도작용급기상관궤제。방법장불동농도적황금감、황금소이급량자연합작용우인유선암(Michigan Cancer Foundation 7，MCF-7)세포。검측상술화합물대유선암세포적활력、조망정황이급조망상관단백표체적영향。결과황금감혹황금소작용우유선암세포후，여작용전상비세포생장억제솔현저승고(P<0.05)；량자연합응용，여량자단독작용상비항증식작용명현증강(P<0.05)。류식세포술검측발현량자작용후우기시량자련용후세포조망현저증가。단백인적분석현시황금감화황금소연합작용후Caspase-3、Caspase-9、Bax화p53적표체증가이Bcl-2표체하강，동시p-38활화역증가。결론황금감화황금소균능유도유선암세포적조망，량자연합응용후작용명현증강，기궤제가능여기촉진촉조망상관단백Caspase-3、Caspase-9、Bax화p53등적표체，병억제항조망단백Bcl-2적표체유관。
Objective To study the breast cancer cell apoptosis is induced by the com bination therapy of baicalin and baicalein and its related m echanism .Methods Different concentrations of baicalin, baicalein and com bined effects of the two drugs in breast cancer MCF-7 cells, test-ing drugs on breast cancer cell viability, apoptosis and apoptosis-related protein expression.Results Baicalin or baicalein acting on the breast cancer cells, cell grow th inhibition was significant-ly higher(P<0.05);com pared with baicalin or baicalein alone, the combination treatm ent with baicalin and baicalein significantly enhanced the anti-proliferative effect (P<0.05).Cell apoptosis was signifi-cantly increased after treating with baicialin or baicalein especially the combination of baicalin and baicalein.Western blot analysis revealed that the expression of Caspase-3, Caspase-9, B ax and p53 were increased.Meanw hile, the level of B cl-2 expression was decreased.Moreover, the activation of p-38 were increased.Conclusions Baicalin and baicalein could induce the apoptosis of breast cancer cells alonely, while the effects significantly enhanced after the combination with baicalin and baicalein. This mechanism may be related with the drugs activate the expression of apoptosis-related protein Caspas-es-3, Caspase-9, Bax and p53, down-regulate the level of Bcl-2, and inhibit the expression of anti-apop-totic protein Bcl-2.