Abstract
目的探讨细胞外信号调节激酶1/2（ERK1/2）抑制剂AZD8330对Burkitt淋巴瘤细胞株Raji细胞的作用及其机制。方法Raji细胞用不同浓度的AZD8330进行处理；采用CCK-8检测细胞存活率；流式细胞术检测细胞凋亡情况；实时定量PCR法检测Bcl-2、Bcl-xl、caspase-3和血管内皮生长因子(VEGF）mRNA表达；Western blot法检测Bcl-2、Bcl-xl、caspase-3、磷酸化(p)-ERK1/2蛋白表达。结果1.00 µmol/L的AZD8330处理24、48和72 h后细胞存活率分别为(62.09±0.86）%、(50.06±1.33）%和(39.13±2.34）%，差异有统计学意义（P值均<0.05）；0.10、1.00、10.00 µmol/L的AZD8330分别处理Raji细胞24、48和72 h，Raji细胞发生凋亡，凋亡率呈时间和剂量依赖性，差异有统计学意义（P值均<0.05）；随着浓度增加和时间延长，Bcl-2、Bcl-xl、VEGF mRNA表达降低，caspase-3 mRNA表达升高，差异有统计学意义（P值均<0.05）；同时，Bcl-2、Bcl-xl、p-ERK1/2蛋白表达明显受抑制，而caspase-3蛋白表达增强。结论AZD8330可能通过抑制ERK1/2通路相关基因和蛋白的表达而诱导Burkitt淋巴瘤Raji细胞凋亡，抑制其增殖。
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