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目的:探讨NF-κB抑制剂在AML白血病发生发展过程中的作用。方法:随机收集16例骨髓标本,其中AML 8例,正常对照8例。应用PCR阵列检测NF-κB信号通路在AML中是否激活?同时构建小鼠白血病模型,检测NF-κB抑制剂对AML的作用。结果:NF-κB信号通路在AML中被激活,在高表达的基因中如EDARADD,TNFSF14可激活NF-κB通路,IL6介导炎症信号;在低表达的基因中如TNFRSF 10B,TNFRSF1A促进细胞凋亡。本实验成功构建了小鼠白血病模型。在小鼠白血病模型中给予NF-κB抑制剂,可缓解白血病微环境对正常造血干细胞的抑制作用,使正常造血干细胞进入细胞周期。结论:AML细胞中NF-κB信号通路被激活,NF-κB抑制剂促进正常造血干细胞细胞进入细胞周期。
Objective: To investigate the role of NF-κB inhibitors in the development of AML leukemia. Methods: 16 cases of bone marrow samples were randomly collected, including 8 cases of AML and 8 cases of normal control. PCR array was used to detect whether NF-κB activation in AML? Simultaneous construction of mouse leukemia model to detect NF-κB inhibitors on AML. Results: The NF-κB signaling pathway was activated in AML. In highly expressed genes such as EDARADD and TNFSF14, NF-κB pathway was activated and IL6 was involved in inflammation. In low expression of genes such as TNFRSF 10B and TNFRSF1A, Death. The experiment successfully constructed mouse leukemia model. In the mouse leukemia model given NF-κB inhibitors, can alleviate the inhibition of leukemic microenvironment of normal hematopoietic stem cells, so that normal hematopoietic stem cells into the cell cycle. CONCLUSION: NF-κB signaling pathway is activated in AML cells and NF-κB inhibitor promotes the entry of normal hematopoietic stem cells into the cell cycle.