目的：探讨鼠尾草酸（CA）通过调节CXC基序趋化因子受体7（CXCR7）/CXC基序趋化因子配体（CXCL12）轴对胃癌AGS细胞增殖、迁移和侵袭的影响。方法：用不同浓度（0、5、10、20、40、80 μg/mL））的CA处理胃癌AGS细胞，采用CCK-8法筛选合适的CA 浓度；将AGS 细胞分为对照组（未经处理的AGS 细胞）、CA 组（20 μg/mL CA 处理）、CA+siCXCR7 组（转染siCXCR7+20 μg/mL CA 处理）、CA+siNC 组（转染siNC+20 μg/mL CA 处理）、CA+vectorNC 组（转染vectorNC+20 μg/mL CA 处理）、CA+vectorCXCR7 组（转染vectorCXCR7+20 μg/mL CA处理），采用CCK-8 法检测AGS 细胞增殖的变化，qPCR 法检测细胞中CXCR7、CXCL12 mRNA表达水平的变化，Transwell 实验检测细胞侵袭能力的变化，划痕实验检测细胞迁移能力的变化，WB法检测周期蛋白D1、Bcl-2、CXCR7、CXCL12、MMP-2蛋白表达的变化。结果：不同浓度CA均可抑制AGS细胞存活率，且浓度为20 μg/mL 时，细胞存活率接近50%，故选择20 μg/mL CA用于后续研究。与对照组相比，CA组增殖率、侵袭数、迁移率、周期蛋白D1、MMP-2、Bcl-2、CXCR7、CXCL12 mRNA及蛋白表达显著降低（均P<0.05）；与CA+siNC 组相比，CA+siCXCR7组增殖率、侵袭数、迁移率、周期蛋白D1、MMP-2、Bcl-2、CXCR7、CXCL12 mRNA及蛋白表达显著降低（均P<0.05）；与CA+vectorNC 组相比， CA+vectorCXCR7组增殖率、侵袭数、迁移率、周期蛋白D1、MMP-2、Bcl-2、CXCR7、CXCL12 mRNA 及蛋白表达显著增加（均P<0.05）。结论：CA可抑制AGS细胞增殖、迁移和侵袭，其机制可能与抑制CXCR7/CXCL12轴有关。

Objective: To investigate the effects of carnosic acid (CA) on the proliferation, migration, and invasion of gastric cancer cells by regulating CXC chemokine receptor 7 (CXCR7)/CXC chemokine ligand 12 (CXCL12) axis. Methods: CCK-8 method was used to select appropriate concentrations of CA. Gastric cancer AGS cells were treated with CA at different concentrations (0, 5, 10, 20, 40, 80 μg/mL). AGS cells were divided into the control group (untreated AGS cells), CA group (20 μg/mL CA treatment), CA+ siCXCR7 group (siCXCR7 transfection+20 μg/mL CA treatment), CA+siNC group (siNC transfection+20 μg/mL CA treatment), CA+ vectorNC group (vectorNC transfection+20 μg/mL CA treatment), and CA+vectorCXCR7 group (vectorCXCR7 transfection+20 μg/mL CA treatment). The proliferation of AGS cells was detected by CCK-8 method; the expression levels of CXCR7 and CXCL12 mRNA in cells were detected by qPCR; and the invasion of cells was detected by Transwell assay; the change of cell migration ability was detected by scratch assay, and the expressions of cyclin D1, Bcl-2, CXCR7, CXCL12 and MMP-2 were detected by WB assay. Results: Different concentrations of CA were all able to inhibit the survival rate of AGS cells. When the concentration was 20 μg/mL, the survival rate of AGS cells was closed to 50%. 20 μg/mL CA was therefore chosen for subsequent research. Compared with the control group, the proliferation rate, invasion number, migration rate, cyclin D1, MMP-2, Bcl-2, CXCR7, CXCL12 mRNA and protein expression of the CA group decreased significantly (all P<0.05). Compared with the CA+siNC group, the proliferation rate, invasion number, migration rate, cyclin D1, MMP-2, Bcl-2, CXCR7, CXCL12 mRNA and protein expression in the CA+siCXCR7 group decreased significantly (all P<0.05). Compared with the CA+vectorNC group, the proliferation rate, invasion number, migration rate, cyclin D1, MMP-2, Bcl-2, CXCR7, CXCL12 mRNA and protein expression in the CA+vectorCXCR7 group increased significantly (all P<0.05). Conclusion: CA can inhibit the proliferation, migration, and invasion of AGS cells, which may be related to the inhibition of CXCR7/CXCL12 axis.