Shu Jun, Zhou Jian-ping
Guangdong General Hospital, Guangzhou 510080, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2010 Jun;26(6):578-9.
To ascertain the role of FK-kappaB in cyclosporine A (CsA)-induced nephrotoxicity in human kidney tubular epithelial cell.
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-kappaB, 25 micromol/L pyrrolidine dithiocarbamate (PDTC) were added respectively. Mitochondria membrane potential were detected by flow cytometry. The activation of NF-kappaB was studied by the assessment of NF-kappaB P65 measured by laser scanning confocal microscope.
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-kappaB but cells in the CsA-induced damage of human kidney tubular epithelial cell. This damage is ameliorated when the activation of NF-kappaB is blockaded.
确定FK-κB在环孢素A（CsA）诱导的人肾小管上皮细胞肾毒性中的作用。
将人肾小管上皮细胞分别用浓度为0、0.1、1、10 mmol/L的CsA处理24小时。分别加入25 μmol/L吡咯烷二硫代氨基甲酸盐（PDTC）作为核因子κB（NF-κB）的抑制剂。通过流式细胞术检测线粒体膜电位。通过激光扫描共聚焦显微镜测量NF-κB P65来研究NF-κB的激活情况。
CsA处理的细胞线粒体膜电位降低，但CsA + PDTC处理的细胞未出现此情况。用CsA处理的细胞激活了NF-κB，但在CsA诱导的人肾小管上皮细胞损伤中，当NF-κB的激活被阻断时，这种损伤得到改善。
