目的 探讨丹酚酸B对结肠癌细胞HCT116增殖、迁移、糖酵解和上皮-间充质转化（EMT）的作用及机制。方法 通过CCK-8实验和克隆形成实验评估丹酚酸B（25、50、100 μmol·L^-1）对结肠癌细胞HCT116增殖的影响；通过创伤愈合实验评估丹酚酸B对HCT116细胞迁移能力的影响；试剂盒法检测丹酚酸B对结肠癌细胞糖酵解及乳酸水平的影响；通过Western blotting法分析丹酚酸B对EMT相关蛋白E-钙黏蛋白（E-cadherin）、N-钙黏蛋白（N-cadherin）、波形蛋白（Vimentin）和Snail，糖酵解相关蛋白葡萄糖转运蛋白1 （GLUT1）、乳酸脱氢酶A （LDHA），p-丝氨酸/苏氨酸激酶（AKT）/核因子κB（NF-κB）信号通路相关蛋白AKT、p-p65的调控作用。结果 与对照组相比，50、100 μmol·L^-1丹酚酸B显著抑制HCT116细胞的增殖（P＜0.01、0.001）；100 μmol·L^-1丹酚酸B显著阻断HCT116细胞的迁移（P＜0.001）； 50、100 μmol·L^-1丹酚酸B显著降低HCT116细胞GLUT1和LDHA的蛋白表达（P＜0.01、0.001），显著降低HCT116细胞的葡萄糖消耗及乳酸产生（P＜0.01、0.001）；50、100 μmol·L^-1丹酚酸B组上皮标志物E-cadherin的蛋白表达显著上升（P＜0.01、0.001），而间充质标志物N-cadherin、Vimentin和转录因子Snail的蛋白表达显著下降（P＜0.01、0.001）；50、100 μmol·L^-1丹酚酸B显著降低AKT的磷酸化水平和核因子κB（NF-κB）的亚基p65的磷酸化水平（P＜0.01、0.001）。结论 丹酚酸B能显著抑制结肠癌细胞的增殖、迁移能力，并有效抑制EMT过程、糖酵解，可能通过抑制AKT/NF-κB信号通路实现。

Objective To investigate the effects of salvianolic acid B on the proliferation, migration, glycolysis, and epithelialmesenchymal transition (EMT) of colon cancer cells HCT116 and the related mechanism. Methods The proliferation of HCT116 cells was evaluated by CCK-8 assay and colony formation assay with salvianolic acid B (25, 50, and 100 μmol·L^-1). The migration ability of HCT116 cells was evaluated by wound healing assay with salvianolic acid B. The glycolysis and lactate levels of HCT116 cells were detected by kit assay. The effects of salvianolic acid B on the EMT-related proteins E-cadherin, N-cadherin, Vimentin, and Snail, the glycolysis-related proteins GLUT1 and LDHA, and the p-serine/threonine kinase (AKT)/nuclear factor kappa B (NF-κB) signaling pathway-related proteins AKT and p-p65 were analyzed by Western blotting. Results Compared with the control group, 50 and 100 μmol·L^-1 salvianolic acid B significantly inhibited the proliferation of HCT116 cells (P < 0.01, 0.001), 100 μmol·L^-1 salvianolic acid B significantly blocked the migration of HCT116 cells (P < 0.001), 50 and 100 μmol·L^-1 salvianolic acid B significantly reduced the protein expression of GLUT1 and LDHA in HCT116 cells (P < 0.01, 0.001), and significantly reduced the consumption of glucose and lactate in HCT116 cells (P < 0.01, 0.001). 50 and 100 μmol·L^-1 of salvianolic acid B treatment resulted in a significant increase in the protein expression of epithelial marker E-cadherin (P < 0.01, 0.001), while the expression of mesenchymal markers N-cadherin, Vimentin, and transcription factor Snail significantly decreased (P < 0.01, 0.001), 50 and 100 μmol·L^-1 of salvianolic acid B significantly reduced the phosphorylation levels of AKT and the subunit p65 of NF-κB (P < 0.01, 0.001). Conclusion Salvianolic acid B can significantly inhibit the proliferation and migration of colon cancer cells, effectively inhibit the EMT process and glycolysis, and may achieve this by inhibiting the AKT/NF-κ B signaling pathway.

R285.5

国家自然科学基金资助项目（81660302）