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作 者:丁晓蓉[1] 喻晓娟[1] 李进[1] 于伟勇[1] 何敬东[1]
机构地区:[1]南京医科大学附属淮安市第一人民医院肿瘤内科,江苏淮安223300
出 处:《临床和实验医学杂志》2016年第15期1496-1499,共4页Journal of Clinical and Experimental Medicine
摘 要:目的探讨CXCR4抑制剂AMD3100、硼替佐米对人淋巴瘤细胞株Ramos协同诱导凋亡作用。方法 1检测淋巴瘤患者骨髓单个核细胞中CXCR4及核因子κB(NF-κB)表达水平;2AMD3100、硼替佐米单用以及联合用药分别处理Ramos细胞,利用CCK-8法检测细胞增殖;利用流式细胞术检测细胞凋亡;Wester blot检测NF-κB、Bcl-2、Bcl-xl、c-IAP1及Caspase-3表达水平。结果 1淋巴瘤患者骨髓单个核细胞中CXCR4、NF-κB表达增高;2AMD3100、硼替佐米作用Ramos细胞后,随着药物浓度的增加,对细胞增殖的抑制作用逐渐增强、凋亡增加,两药具有协同作用(P<0.05);3AMD3100、硼替佐米单药组NF-κB、Bcl-2、Bcl-xl及c-IAP1表达降低,Caspase-3表达升高,联合用药组作用增强。结论 AMD3100、硼替佐米对Ramos细胞的增殖抑制、凋亡促进具有协同作用,其作用机制可能是通过抑制NF-κB、Bcl-2、Bcl-xl、c-IAP1及增强Caspase-3表达。Objective To investigate the synergistic effects of CXCR4 inhibitors AMD3100 and Bortezomib on apoptosis of lymphoma cell lines Ramos. Methods ①The detection of CXCR4 and NF - κB on bone marrow mononuclear cells of lymphoma patients;②The cells were trea-ted with AMD3100,Bortezomib,AMD3100 combined with Bortezomib,respectively. The proliferation was estimated by CCK - 8,the cell apopto-sis was analysed by flow cytometry,the expression level of NF - κB,Bcl - 2,Bcl - xl,c - IAP1 and Caspase - 3 were measured by Western blot. Results ①The CXCR4 and NF - κB were both highly expressed in bone marrow mononuclear cells of lymphoma patients. ②Both AMD3100 and Bortezomib can inhibit the proliferation and promote apoptosis of Ramos cell,the effect showed dosage dependent manner,AMD3100 and Borte-zomib had the synergy effects( P ﹤ 0. 05). ③The expression level of NF - κB,Bcl - 2,Bcl - xl and c - IAP1 were lower in the single drug and combination groups,but the expression of Caspase - 3 was in the different way. Conclusion AMD3100 and Bortezomib has synergistic effect in the proliferation and apoptosis of Ramos cell line,the mechanism of the effects may be down - regulated the expression level of NF - κB,Bcl - 2, Bcl - xl,c - IAP1and up - regulated the expression of Caspase - 3.
关 键 词:CXCR4抑制剂AMD3100 硼替佐米 淋巴瘤 Ramos细胞株 细胞凋亡
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