三氧化二砷诱导白血病细胞凋亡与核因子-κB活化的关系

为了研究三氧化二砷（As2O3）诱导白血病细胞凋亡与核因子-κB（NF-κB）活化以及血管内皮生长因子（VEGF）、基质金属蛋白酶-9（MMP9）表达的关系,应用流式细胞仪Annexin V FITC法检测白血病细胞系K562-n凋亡;采用免疫组织化学方法半定量分析K562-n细胞NF-κB、VEGF、MMP9表达的动态变化.结果显示：As2O3在诱导K562-n细胞凋亡的过程中可活化NF-κB,而VEGF、MMP9的表达也随之增强.地塞米松（DXM）1μmol/L能显著增加As2O3诱导K562-n细胞凋亡的作用和抑制K562-n细胞NF-κB活化,细胞凋亡增加率为43.04%,（P＜0.05）,NF-κB活化抑制率为31.15%（P＜0.05）,VEGF、MMP9变化与NF-κB一致.结论：As2O3诱导K562-n细胞凋亡的过程中可使NF-κB活化,VEGF、MMP9表达亦随之增强;DXM可通过抑制NF-κB活化增强其诱导K562-n细胞凋亡的作用,VEGF、MMP9的表达也随之下降.

Arsenic Trioxide Induced Leukemic Cell Apoptosis Relative to NF-κB Activation

To investigate the relationship of As(2)O(3)-induced leukemic cell apoptosis with NF-kappaB activation and expression of VEGF, MMP9, apoptosis of K562-n cells induced by As(2)O(3) was analyzed by Annexin V, the dynamic changes of NF-kappaB, MMP9 and VEGF expressions were detected by immunohistochemistry. The results showed that activity of NF-kappaB could be increased, accompanied by higher level of expression of MMP9 and VEGF when apoptosis of K562-n cells was induced by As(2)O(3). Dexamethasome not only increased significantly the apoptotic rate, but also suppressed the activation of NF-kappaB of K562-n cells induced by As(2)O(3). Furthermore, there was a positive correlation between the expression of MMP9, VEGF and the activity of NF-kappaB. It is concluded that As(2)O(3) can induce apoptosis, in the meanwhile, activate NF-kappaB and up-regulate expression of MMP9 and VEGF in K562-n cell line. The mechanism of apoptosis of K562-n cells enhanced by dexamethasome may be related to suppression of the activation of NF-kappaB and expression of MMP9 and VEGF.