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目的建立肺微血管内皮三维培养系统,观察抗血管内皮生长因子(VEGF)的人源化单克隆抗体Avastin对肺癌诱导的肺微血管生成的效应,并探讨其作用机制。方法通过血管生成抑制实验和采用流式细胞仪检测细胞周期和凋亡率的变化,观察Avastin对肺微血管内皮细胞的影响。结果随着Avastin作用浓度的增加,无血管结构区域的面积亦增加,由25μg/ml时的(0.944±0.073)cm2增加为100μg/ml的(5.189±0.192)cm2,凋亡率亦由(32.5±1.5)%增加为(39.2±1.6)%,并阻滞LVEC于G0/1期边界,造成细胞周期停滞,同时引起S期和G2/M期细胞比例显著降低。结论Avastin可抑制肺癌诱导的肺微血管内皮细胞的生长,并诱导细胞凋亡的发生,可能与Avastin阻滞LVEC于G0/1期边界,造成细胞周期停滞有关。
Objective To establish a three-dimensional culture system of pulmonary microvascular endothelial cells and observe the effect of Avastin, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF) on pulmonary microvascular angiogenesis induced by lung cancer and to explore its mechanism. Methods The effects of Avastin on pulmonary microvascular endothelial cells were observed by means of angiogenesis inhibition assay and flow cytometry to detect cell cycle and apoptosis rate. Results With the increase of the concentration of Avastin, the area of non-vascular structure also increased, from (0.944 ± 0.073) cm2 at 25μg / ml to (5.189 ± 0.192) cm2 at 100μg / ml, ± 1.5%) to (39.2 ± 1.6)%, and blocked LVEC at the G0 / 1 boundary, resulting in cell cycle arrest and a significant decrease in the proportion of cells in S phase and G2 / M phase. Conclusion Avastin can inhibit lung cancer-induced pulmonary microvascular endothelial cell growth and induce apoptosis, which may be related to Avastin blocking LVEC at the G0 / 1 boundary, resulting in cell cycle arrest.