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目的研究三氧化二砷(As2O3)在体外对人类伯基特氏淋巴瘤细胞凋亡的影响,并探讨其作用机制。方法分别采用来源于人类伯基特氏淋巴瘤的EB病毒阳性细胞Raji和EB病毒阴性细胞BJAB为模型,利用细胞形态学检测、DNA凝胶电泳和蛋白质Western blotting分析等方法,从细胞形态、DNA水平和蛋白质水平探讨As2O3诱导恶性淋巴瘤凋亡及作用机制。结果分别采用2, 5和10 mol/L的As2O3与Raji和BJAB细胞作用24 h后,DNA凝胶电泳证实As2O3通过诱导细胞凋亡而抑制细胞的增殖。BJAB和Raji细胞对应于上述浓度As2O3的凋亡率分别47.6%±4.8% (Mean±SD, n=3), 66.4%±5.1% , 87.0%±7.3% 和35.5%±3.8%, 51.5%±6.2%, 62.2%±7.9,BJAB细胞对As2O3的敏感性要高于Raji细胞(P<0.05)。Western blotting蛋白质检测表明,As2O3通过下调抗凋亡蛋白Bcl-xL的表达和激活凋亡分子caspase-3诱导细胞凋亡。结论As2O3通过下调Bcl-xL蛋白的表达和激活caspase-3诱导人类恶性淋巴瘤细胞的凋亡;本研究可望为临床应用砷剂治疗恶性淋巴瘤提供实验依据。
Objective To study the effect of arsenic trioxide (As2O3) on apoptosis of human Burkitt’s lymphoma in vitro and to explore its mechanism. Methods The Epstein-Barr virus-positive cells Raji and EBV-negative cells BJAB derived from human Burkitt’s lymphoma were used as models. Cell morphology, DNA gel electrophoresis and Western blotting were used to analyze the cell morphology, DNA Level and protein levels in As2O3-induced apoptosis of malignant lymphoma and its mechanism. Results After treated with 2, 5 and 10 mol / L As2O3 for 24 h with Raji and BJAB cells respectively, DNA gel electrophoresis confirmed that As2O3 could inhibit cell proliferation by inducing apoptosis. The apoptosis rates of BJAB and Raji cells corresponding to the above concentrations of As2O3 were 47.6% ± 4.8% (Mean ± SD, n = 3), 66.4% ± 5.1%, 87.0% ± 7.3% and 35.5% ± 3.8%, 51.5% ± 6.2%, 62.2% ± 7.9. The sensitivity of BJAB cells to As2O3 was higher than that of Raji cells (P <0.05). Western blotting showed that As2O3 could induce apoptosis by down-regulating the expression of anti-apoptotic protein Bcl-xL and activating caspase-3. Conclusion As2O3 can induce the apoptosis of human malignant lymphoma cells by down-regulating the expression of Bcl-xL protein and activating caspase-3. This study is expected to provide experimental evidence for the clinical application of arsenic in the treatment of malignant lymphoma.