方法：用不同浓度(0、0.625、1.25、2.5、5.0mg/mL)的贝伐单抗干预体外培养人视网膜色素上皮细胞ARPE-19，采用CCK-8法分别于24、48、72h检测细胞活性； 流式细胞仪检测细胞周期； 应用免疫蛋白印迹法(Western blotting)及逆转录聚合酶链反应(RT-PCR)检测ARPE-19中E-cadherin和fibronectin的蛋白及mRNA的表达变化。

结果：浓度为2.5、5.0mg/mL贝伐单抗能有效抑制ARPE-19细胞的增殖及细胞周期，差异有统计学意义(P<0.05)。2.5、5.0mg/mL贝伐单抗能抑制E-cadherin基因，促进fibronectin基因的转录及表达，差异有统计学意义(P<0.05)。

结论：高浓度的贝伐单抗能够抑制ARPE-19细胞的增殖，下调纤维化相关因子E-cadherin，同时上调fibronectin的表达，提示高浓度的贝伐单抗可以引起ARPE-19细胞纤维化。

METHODS: Different concentrations(0, 0.625, 1.25, 2.5, 5.0mg/mL)of bevacizumab were exposed to ARPE-19 cells, then cell viability was analyzed by CCK-8, cell cycle was determined by flow cytometry, and the expression of E-Cadherin and fibornectin was detected by Western blot and RT-PCR.

RESULTS: The concentration as 2.5mg/mL or 5.0mg/mL of bevacizumab was shown to effectively suppress the proliferation and cell cycle of ARPE-19 cell(P<0.05). In addition, 2.5mg/mL or 5.0mg/mL of bevacizumab could downregulate the expression of E-cadherin and promote the transcription of fibronection gene(P<0.05).

CONCLUSION: High concentration of bevacizumab was able to inhibit ARPE-19 proliferation, downregulate E-Cadherin expression and promote fibronectin expression, indicating epithelial-mesenchymal transition induced by bevacizumab in ARPE-19 cell.