激素敏感型单纯性肾病病毒基因反式激活调控中IκBα的异常表达

Abnormal expression of IκBα during viral transactivation of transcription in steroid responsive simple nephrotic syndrome

目的研究激素敏感型单纯性肾病(SRSNS)病毒基因反式激活过程中IκBα基因表达及其对NF-κB活性的调控作用。方法采用实时定量RT-PCR、Westernblot和电泳迁移率改变实验、RT-PCR和ELISA分别检测SRSNS活动期、缓解期患儿和正常儿童外周血单个核细胞(PBMCs)中IκBαmRNA、IκBα蛋白质、NF-κB活性、呼吸道病毒基因表达和血浆病毒抗体。结果SRSNS活动期NF-κB活性高于SRSNS缓解期和正常儿童,与呼吸道病毒检出率呈正相关趋势;SRSNS活动期IκBα蛋白质低于SRSNS缓解期患儿和正常儿童,与NF-κB活性呈直线负相关(r=-0.884,P<0.05)。而SRSNS活动期IκBαmRNA水平高于正常儿童,但仍低于SRSNS缓解期。结论SRSNS病毒基因反式激活过程中存在IκBα异常表达,IκBα蛋白质调控NF-κB活性。

Objective, To investigate IκBa expression and its role in regulating the activity of NF-κB during viral transactivation of transcription in steroid responsive simple nephrotic syndrome （SRSNS） , Methods： Children with SRSNS （including active and remissive stage） were examined , and healthy children were chosen as controls. Real time RT-PCR, Western blot ,electro-mobility shift assays, RT-PCR and ELISA were performed to study the gene and protein expression of IκBa , the activity of NF-κB , the gene expression of respiratory tract viruses （ including respiratory syncytial virus and influenza virus） in peripheral blood mononuclear cells （PBMCs） and viral antibody in plasma , respectively . Results, SRSNS at active stage displayed higher levels of NF-κB activity , compared to SRSNS at remission stage and healthy children. Positive correlation between the activity of NF-κB and the gene expression of respiratory tract viruses was observed. In addition, levels of IκBa protein from SRSNS at active stage were much lower than those from healthy children and those from SRSNS at remissive stage. There was a linear negative correlation between the activity of NF-κB and the level of IκBa protein （r = - 0. 884, P〈0.05）. On the other hand, levels of IκBa mRNA from SRSNS at active stage were much higher than those from healthy children, but much lower than those from SRSNS at remissive stage. Conclusion Abnormal expression of IκBa , which contributes to the regulation of the activity of NF-κB, occurs in viral transactlvation of transcription triggered by respiratory tract viruses in SRSNS .