利多卡因抑制内皮细胞粘附因子表达进而抑制肝癌细胞粘附脐带静脉内皮细胞

Lidocaine inhibits the adhesion of HepG2 to human umbilical vein endothelial cells by modulated endothelial cell adhesion molecules

目的探讨利多卡因对血管内皮细胞粘附因子表达的影响。方法采用不同浓度利多卡因预处理脐带静脉内皮细胞(HUVECs)30 min后,加入肿瘤坏死因子α(TNFα)进行刺激。通过实时荧光定量聚合酶链反应检测选择素E(CD62E)、血管细胞粘附分子-1(VCAM-1)和细胞间粘附分子-1(ICAM-1)表达量,蛋白免疫印迹分析NF-Kappa B(NF-κB)通路蛋白的改变,并通过细胞粘附实验评估利多卡因预处理对肝癌细胞(Hep G2)粘附于HUVECs的影响。结果利多卡因预处理可以明显抑制p65并抑制Hep G2粘附于HUVECs。q RT-PCR结果表明利多卡因预处理可明显抑制TNF-α刺激后的CD62E、VCAM-1和ICAM-1表达水平的增高。结论利多卡因可能通过抑制NF-κB通路进而抑制细胞粘附因子表达并抑制结肝癌细胞粘附于血管内皮细胞。

Objective To explore the effect of lidocaine on endothelial cell adhesion molecules.Methods Human umbilical vein endothelial cells（HUVECs） were preincubated with different concentration of lidocaine prior to tumor necrosis factor（TNFα,10 ng·ml^-1）for different time. Tumour cell adhesion assays were performed. The m RNA of endothelial- selectin（E- Selectin,CD62E）,intercellular adhesion molecule- 1（ICAM- 1）and vascular cell adhesion molecule- 1（VCAM- 1）were detected via quantitative reverse-transcriptase polymerase chain reaction（q RT-PCR）. The proteins of p65 were evaluated via western blotting. Results Compared with TNFα,the adhesion of HepG2 was significantly inhibited by lidocaine. CD62 E,VCAM-1 and ICAM-1 expression were significantly promoted by TNFα. After pretreatment of lidocaine for 30 min,CD62 E,VCAM-1 and ICAM-1 expression were significantly inhibited. Meanwhile,the phosphorylation of p65 were significantly attenuated by lidocaine.Conclusion Our results suggested that lidocaine modulated the expression of endothelial cell adhesion molecules and inhibited the adhesion of cancer cell.