目的:研究甘草查尔酮B(licochalcone B,LCB)对人乳腺癌细胞MCF-7的增殖抑制作用,并初步探讨其作用机制。方法:取对数生长期MCF-7细胞按6×104个/孔接种于6孔板中,台盼蓝拒染法检测MCF-7细胞的生长曲线并计算细胞倍增时间;取对数生长期MCF-7细胞按1×104个/孔接种于96孔板中,噻唑蓝(MTT)法检测甘草查尔酮B(0,10,20,40,60,80μmol·L-1)作用24,48,72 h后,对MCF-7细胞的增殖抑制作用;取对数生长期MCF-7细胞按2×105个/孔接种于6孔板中,LCB(0,20,40,80μmol·L-1)作用48 h后,显微镜下观察细胞形态;取对数生长期MCF-7细胞按2×105个/孔接种于6孔板中,LCB(0,20,40,80μmol·L-1)作用48 h后,Hoechst 33258染色法观察细胞凋亡形态;取对数生长期MCF-7细胞按9×105个/瓶接种于细胞培养瓶中,LCB(0,20,40,80μmol·L-1)作用48 h后,流式细胞仪检测细胞凋亡率,实时荧光定量聚合酶链式反应(q PCR)法检测与凋亡相关基因B细胞淋巴瘤/白血病-2(Bcl-2)相关X蛋白(Bax),Bcl-XL,半胱氨酸天冬氨酸蛋白酶-3(Caspase-3),Caspase-9转录水平的变化。结果:与0μmol·L-1LCB组比较,LCB能够以时间和浓度依赖性方式有效的抑制MCF-7细胞增殖,经LCB处理后的MCF-7细胞呈现出染色体边集、核浓缩、核碎裂等典型凋亡形态学特征,细胞凋亡率随着LCB浓度的增加而升高,且LCB能明显下调Bcl-XL,上调Bax,Caspase-3,Caspase-9的表达(P<0.05,P<0.01)。结论:LCB在体外能显著抑制MCF-7细胞增殖,具有诱导MCF-7细胞凋亡的作用,其机制可能与药物上调Bax,下调Bcl-XL,激活由Caspase-3,Caspase-9介导的线粒体凋亡信号通路有关。 OBJECTIVE: To study the inhibitory effect of licochalcone B (LCB) on the proliferation of human breast cancer cell line MCF-7 and to explore its mechanism. Methods: The logarithmic growth phase of MCF-7 cells were seeded into 6-well plates at 6 × 104 cells / well, and the growth curve of MCF-7 cells was detected by trypan blue exclusion method. The logarithmic growth phase MCF-7 cells were seeded into 96-well plates at a density of 1 × 10 4 / well, and the effect of licochalcone B (0, 10, 20, 40, 60 and 80 μmol·L -1) 48,72 h after MCF-7 cells proliferation inhibition; take logarithmic growth phase MCF-7 cells by 2 × 105 / well in 6-well plates, LCB (0,20,40,80μmol·L 1) for 48 h, the morphology of cells was observed under the microscope. The logarithmic growth phase of MCF-7 cells was seeded into 6-well plates at a density of 2 × 105 cells / well and LCB (0, 20, 40, 80μmol·L- ) For 48 h, the morphology of apoptotic cells was observed by Hoechst 33258 staining; MCF-7 cells were seeded into cell culture flasks at a density of 9 × 105 cells / mL in LCB (0, 20, 40, 80 μmol·L -1) for 48 h, the apoptotic rate was detected by flow cytometry and the correlation with the apoptosis related gene B-cell lymphoma / leukemia-2 (Bcl-2) Related protein B (Bax), Bcl-XL, Caspase-3 and Caspase-9. Results: Compared with 0μmol·L-1 LCB group, LCB could effectively inhibit the proliferation of MCF-7 cells in a time-and concentration-dependent manner. The LCB-treated MCF-7 cells showed the chromatin margination, nuclear condensation, (P <0.05, P <0.05). The apoptotic rate increased with the increase of LCB concentration. LCB could down-regulate Bcl-XL and up-regulate the expression of Bax, Caspase-3 and Caspase- 0.01). CONCLUSION: LCB can significantly inhibit the proliferation of MCF-7 cells in vitro and induce the apoptosis of MCF-7 cells. The mechanism may be related to the up-regulation of Bax, the down-regulation of Bcl-XL and the activation of Caspase-3 and Caspase-9 Mitochondrial apoptosis signaling pathway.