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目的 研究三氧化二砷(As2O3 )诱导淋巴瘤细胞凋亡与核因子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,并观察地塞米松(Dex)抑制NF κB活化对As2O3诱导淋巴瘤细胞凋亡及VEGF、MMP9表达的影响。方法 采用流式细胞仪AnnexinⅤFITC法检测Raji细胞凋亡;采用免疫组织化学方法半定量分析Raji细胞NF κB、VEGF、MMP9表达的动态变化。结果 As2O3同时具有诱导Raji细胞凋亡[凋亡率为(39. 2±1. 3)% ]和NF κB活化的作用; 1. 0μmol/LDex能显著增加1 . 0μmol/LAs2O3诱导Raji细胞凋亡(增加率为77. 5%,P<0. 05)和抑制As2O3诱导Raji细胞NF κB活化(抑制率为28. 0%,P<0. 05)的作用,VEGF、MMP9变化与NF κB一致。结论 As2O3诱导Raji细胞凋亡的同时活化NF κB,VEGF、MMP9表达亦随之增强;Dex在抑制As2O3诱导Raji细胞NF κB活化的同时增强其诱导细胞凋亡的作用,VEGF、MMP9的表达也相应下降。
Objective To investigate the relationship between the apoptosis of lymphoma cells induced by As2O3 and the activation of nuclear factor κB (NF κB) and the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 9 (MMP9), and to observe the effect of Dex Effect of NF κB activation on As2O3 - induced apoptosis of lymphoma cells and expression of VEGF and. Methods The apoptosis of Raji cells was detected by flow cytometry Annexin Ⅴ FITC. The dynamic changes of NF-κB, VEGF and MMP9 in Raji cells were detected by immunohistochemistry. Results As2O3 also induced Raji cell apoptosis [(39.2 ± 1.3)%] and NFκB activation. 1. 0μmol / L Dex significantly increased Raji cell apoptosis by 1.0μmol / L As2O3 (77.5%, P <0.05) and inhibition of As 2 O 3 -induced activation of NF κB in Raji cells (the inhibition rate was 28.0%, P <0.05). The changes of VEGF and MMP9 were consistent with those of NF κB . Conclusion As2O3 can induce the apoptosis of Raji cells and activate NF-κB simultaneously. The expression of VEGF and MMP-9 is also enhanced. Dex can inhibit the activation of NF-κB in Raji cells and enhance the apoptosis of Raji cells. decline.