摘要
目的探讨尿毒症时主动脉局部炎症信号NF-κB表达变化。方法采用单肾切除、对侧肾动脉部分结扎法建立慢性肾衰竭模型,RT-PCR检测NF-κB p65亚基、I-κB mRNA表达水平,免疫组织化学检测p65亚基蛋白表达,凝胶迁移率法测定NF-κB活性,并用图像分析定量。结果与正常大鼠比较,慢性肾衰竭大鼠主动脉NF-κB p65亚基mRNA表达水平显著升高(P<0.01),而I-κB mRNA表达水平显著降低(P<0.01),NF-κB p65亚基蛋白表达和活性也显著增加(P<0.01),并随病程延长而进一步上升。蛋白酶体抑制剂MG-132可明显抑制慢性肾衰竭大鼠主动脉NF-κB组分表达和活性升高。结论慢性肾衰竭大鼠主动脉NF-κB炎症信号通路存在显著活化。
Objective To chronic renal failure. Methods investigate the alteration of inflammatory signal （NF-KB） in aorta of rats with The animal model was established by partial ligation of renal pedical artery and other side nephrectomy. The mRNA expression of NF-κB and I-κB were detected by RT-PCR, the protein expression of NF-κB was measured by immunohistochemistry, and the activity of NF-κB was examed by electro- phoresis mobility shift assay（EMSA）. Results Significant increase of the mRNA expression of NF-κB p65 was found in experimental group than in control group（P 〈0. 01 ）, while marked decrease of the mRNA expression of I-κB was noted（P 〈0. 01 ）. The protein expression and activity of NF-κB was also increased significantly（P 〈0. 01 ） , and it is further increased in the course of renal failure progress. The expression and activity of NF-κB was inhibited significantly by MG-132 treatment. Conclusion The inflammatory signal of NF-κB is activated in the pathogenesis of chronic renal failure of rats.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2008年第15期1430-1433,共4页
Journal of Third Military Medical University
基金
国家自然科学基金(30570763)~~
