目的：探讨甘草查尔酮B（LCB）对三阴性乳腺癌（TNBC）MDA-MB-231 细胞的抑制作用及其机制。方法: 常规培养MDA-MB-231 细胞，用不同浓度LCB 处理后，采用CCK-8法、免疫荧光法、FCM 和WB法分别检测MDA-MB-231 细胞的增殖活力、细胞核内DNA双链断裂标志物γ-H2AX的表达，以及细胞周期和周期调控、丝裂原活化蛋白激酶（MAPK）、内质网应激信号途径相关蛋白的表达水平。结果: LCB能显著抑制乳腺癌MDA-MB-231 细胞的增殖活力（P<0.05），使γ-H2AX阳性细胞数和蛋白表达水平均显著升高（均P<0.05）、G2/M 和S 期的细胞数量均明显增加（均P<0.05）、MAPK 家族主要成员细胞外调节激酶1/2（ERK1/2）和p38MAPK蛋白的磷酸化水平均显著上调（均P<0.05），还使内质网应激途径相关蛋白Bip、ATF4和CHOP 的表达均显著上调（均P<0.05）。结论: LCB 能够显著抑制MDA-MB-231 细胞的增殖活力、诱导DNA损伤和细胞周期阻滞于G2/M 和S期，LCB对MDA-MB-231细胞的抑制作用可能与其激活MAPK和内质网应激信号通路相关。

Objective: To investigate the inhibitory effect of Licochalcone B (LCB) on a triple-negative breast cancer cell line MDA-MB-231 cells and its mechanism. Methods: MDA-MB-231 cells were routinely cultured and treated with different concentrations of LCB, and then CCK-8 assay, immunofluorescence, FCM and WB analysis were used to detect the proliferative viability of MDA-MB-231 cells, the expression of γ-H2AX, a marker of DNA double-strand breaks in the nucleus, the cell cycle，and the expression levels of proteins related to cycle regulation, mitogen-activated protein kinase (MAPK), and the endoplasmic reticulum stress (ER stress),respectively. Results: LCB significantly inhibited the proliferative viability of breast cancer MDA-MB-231 cells (all P<0.05), the number of γ-H2AX-positive cells and protein expression levels were significantly increased after LCB treatment (all P<0.05), the number of cells in G2/M and S phases was significantly increased (all P<0.05), the phosphorylation levels of the main members of the MAPK family,extracellular regulated kinase 1/2 (ERK1/2) and p38 MAPK phosphorylation levels were significantly upregulated (all P<0.05), and the expression of ER stress pathway-related proteins Bip, ATF4 and CHOP were significantly upregulated (all P<0.05). Conclusion: LCB could significantly inhibit the proliferation vitality of MDA-MB-231 cells and induce DNA damage and cell cycle arrest at G2/M and S phases.The inhibitory effect of LCB on MDA-MB-231 cells may be related to the activation of MAPK and ER stress signaling pathway.

山东省自然科学基金（No. ZR2018MH026）；泰安市科技创新发展项目（No. 2022NS322，No. 2022NS353）