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目的 观察克拉霉素 (CAM)对人小细胞肺癌细胞表达VEGF其诱导血管内皮细胞迁移的影响 ,探讨CAM抗血管生成的机制。方法 采用免疫组化和图象分析技术 ,观察不同浓度的CAM作用下人小细胞肺癌细胞 (NCI -H4 4 6 )中VEGF蛋白表达的变化。采用共培养法 (Marigelinvasioncham ber) ,观察CAM对NCI -H4 4 6细胞诱导人血管内皮细胞(ECV - 30 4 )迁移的抑制作用。结果 CAM达到 30mmol/L对其诱导的ECV - 30 4细胞迁移表现出明显的抑制作用 ,达到 4 0mmol/L可以抑制NCI -H4 4 6细胞表达VEGF ,CAM浓度在 30、4 0和 5 0mmol/L时 ,抑制率分别为 19.7%、2 4 .3%和2 5 .0 % ,呈现出明显剂量—反应关系 (r =- 0 .76 4 ,P =0 .0 0 1)。结论 CAM能够抑制肺癌细胞诱导的血管内皮细胞迁移 ,对其表达VEGF也具有抑制作用 ,以上作用可能是CAM抗血管生成的机制之一。
Objective To investigate the effect of clarithromycin (CAM) on the expression of vascular endothelial growth factor (VEGF) in human small cell lung cancer cells and to explore the mechanism of CAM antiangiogenesis. Methods Immunohistochemistry and image analysis techniques were used to observe the changes of VEGF protein expression in human small cell lung cancer cells (NCI -H4 4 6) treated with different concentrations of CAM. The inhibitory effect of CAM on the migration of human vascular endothelial cells (ECV - 30 4) induced by NCI-H4 4 6 cells was observed by the method of co-culture (Marigelinvasioncham ber). Results The CAM reached 30mmol / L, which could significantly inhibit the ECV - 30 4 cell migration. When 40mmol / L CAM could inhibit the expression of VEGF in NCI - H4 4 6 cells, the concentration of CAM was 30, 40 and 50mmol / L, the inhibition rates were 19.7%, 24.3% and 25.0%, respectively, showing a significant dose-response relationship (r = - 0.764, P = .0 0 1). Conclusions CAM inhibits the migration of vascular endothelial cells induced by lung cancer cells and inhibits the expression of VEGF. These effects may be one of the mechanisms of CAM anti-angiogenesis.