核因子kB抑制剂Bay11—7082和^131I导致DTC细胞凋亡的效果及协同作用

目的：探讨分析核因子kB抑制剂Bayll—7082和^131I导致甲状腺癌（DTC）细胞凋亡的效果及协同作用。方法：对DTc细胞分别进行^131I、Bay11—7082以及两者联合处理，β-actin作为内参对照，采用Westernblot鉴定三种方式处理后，分析细胞内NF—KB调控的凋亡抑制因子以及凋亡关键因子相对表达水平的变化情况。结果：^131I处理后xIAP与survivin的表达，与对照组相比提高，差异具有统计学意义（P〈0．05），经^131I联合Bay11-7082处理后xIAP与survivin的表达，与对照组相比降低，差异具有统计学意义（P〈0．05）；经^131I处理、Bay11-7082处理以及^131I联合Bay11-7082处理后，分别与对照组caspase3的2个亚基p19和p17以及PARP失活水解产物p89相比，均显著上升；与对照组的PARP活性蛋白pll6比较，显著降低，差异均具有统计学意义（P〈0．05）。结论：甲状腺癌细胞内凋亡抑制因子经^131I联合Bay11—7082处理后可以明显抑制凋亡抑制因子表达升高的表现，对^131I导致细胞的凋亡产生协同效应。

Effect of NF-kB inhibitor BAY11-7082 and ^131I of inducing apoptosis of cells of differentiated thyroid cancer and their synergistic effects

Objective： To investigate and analyze effect of NF-kB inhibitor BAY11-7082 and ^131I of inducing apoptosis of cells of differentiated thyroid cancer and their cooperative action. Methods. Cells of DTC are processed by the treatment of BAY11-7082, ^131I and the joint treatment of the two. The changes of the relative expression level of the inhibitory factor （surviving, XIAP） and the critical factor （PARP, easpase3） of apoptosis which are regulated by NF-kB are identified by Western blot method. And 13-actin is considered as the internal control. Results： Compared with the control group, the expressions of XIAP and surviving significantly increased （P〈0. 05） after the treatment of ^131I, but significantly reduced （P〈 0.05）after the joint treatment of ^131Iand Bay 11-7082. Compared with the control group, p19 and p17, two subunits of easpase3 and p89 which were the deactivation hydrolysate of PARP significantly increased （P〈0.05） after the treatment of BAY11-7082, ^131I and the joint treatment of ^131I and Bay 11-7082, and pl16 which is the active proteins of PARP significantly reduced （P〈0. 05）. Oonclusion： The expression level of the inhibitory factor of apoptosis in cells of DTC significantly increased after the treatment of ^131I, but the expression of the inhibitory factor of apoptosis is inhibited after the joint treatment of Bayll-7082 and ^131I indicating, the joint treatment of Bay11-7082 and ^131I have synergistic effects on leading to the apoptosis of cell.