核因子-κB在环孢素A致人肾小管上皮细胞损伤中的作用

Role of nuclear factor kappa B in cyclosporine A-induced nephrotoxicity in human tubular epithelial cell

目的:探讨NF-κB在环孢素A(CsA)致肾毒性中的作用。方法:实验共分3组:CsA组,CsA+PDTC组及正常对照组,分别以CsA浓度为0、0.1、1、10mmol/L作用于培养的人肾小管上皮细胞,其中加入NF-κB抑制剂吡咯烷二硫代氨基甲酸(PDCT)。用流式细胞术检测细胞线粒体膜电位的变化;用免疫组化结合激光共聚焦扫描显微镜检测NF-κB。结果:CsA组细胞线粒体膜电位下降,加入PDTC膜电位没有下降。CsA激活人肾小管上皮细胞NF-κB表达。结论:在CsA导致的肾小管上皮损伤中NF-κB被激活,阻断它的激活能减轻损伤的发生。

AIM：To ascertain the role of NF-κB in cyclosporine A（ CsA）-induced nephrotoxicity in human kidney tubular epithelial cell. METHODS： Human kidney tubular epithelial cells were treated with CsA at concentrations of 0, 0.1, 1, 10 mmol/L for 24 hours. As inhibitors of NF-κB, 25 μmol/L pyrrolidine dithiocarbamate（PDTC） were added respectively. Mitochondria membrane potential was detected by flow cytometry. The activation of NF-κB was studied by the assessment of NF-κB P65 measured by laser scanning confocal microscope. RESULTS： Mitochondrial membrane potential showed a decrease in the cells with CsA, but the cells with CsA＋PDTC did not.cells treated with CsA activated NF-κB but cells with PDTC did not. CONCLUSION： NF-κB is activated in the CsA-induced damage of human kidney tubular epithelial cell, This damage is ameliorated when the activation of NF-κB is blockaded.