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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。
Objective: To investigate the role of NF-κB in renal toxicity induced by cyclosporine A (CsA). Methods: The experiment was divided into three groups: CsA group, CsA + PDTC group and normal control group. The cultured human renal tubular epithelial cells were treated with CsA at the concentrations of 0, 0.1, 1 and 10 mmol / L, respectively. Agent pyrrolidine dithiocarbamate (PDCT). The changes of mitochondrial membrane potential were detected by flow cytometry. NF-κB was detected by immunohistochemistry and confocal laser scanning microscopy. Results: The mitochondrial membrane potential of CsA group decreased and the membrane potential of PDTC was not decreased. CsA Activates NF-κB Expression in Human Renal Tubular Epithelial Cells. Conclusion: NF-κB is activated in renal tubular epithelial cells induced by CsA, blocking its activation can reduce the occurrence of injury.