Avastin对肺癌诱导的肺微血管生成的影响

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。

Bevacizumab (Avastin) inhibits lung cancer-induced pulmonary microvascular angiogenesis

OBJECTIVE: To study the effect of bevacizumab (Avastin) on pulmonary microvascular angiogenesis induced by lung cancer. METHODS: The effects of Avastin on cell growth, cell cycle and apoptosis of lung microvascular endothelial cells were assayed by flow cytometry. RESULTS: Avastin inhibited the growth of lung microvascular endothelial cells and induced increase of cell apoptosis index in a concentration-dependent manner. With the increment of Avastin concentration from 25 to 100 microg/ml, avascular area increased from 0.944-/+0.073 cm square to 5.189-/+0.192 cm square, and the cell apoptosis index increased from 32.5%-/+1.5% to 39.25-/+1.6%. CONCLUSION: Avastin can inhibit the growth and induce apoptosis of lung microvascular endothelial cells in three-dimensional culture, possibly in association with cell cycle arrest in G(0/1) phase.