血管紧张素Ⅱ诱导肾小管上皮细胞损伤的实验研究

目的:研究血管紧张素Ⅱ诱导肾小管上皮细胞损伤的机制。方法:血管紧张素Ⅱ(10-7μmol/l)加入肾小管上皮细胞为对照组;体外培养的肾小管上皮细胞作为空白对照;不同浓度缬沙坦(10-6μmol/l、10-7μmol/l、10-8μmol/l、10-9μmol/l)先与肾小管上皮细胞共同培养半小时后再加入血管紧张素Ⅱ(10-7μmol/l)为干预组;EMSA、RT-PCR分别检测不同时限NF-κB活性、骨桥蛋白mRNA表达。结果:血管紧张素Ⅱ可诱导肾小管上皮细胞内NF-κB活性增加,骨桥蛋白mRNA表达上调;而不同浓度缬沙坦干预组检测结果显示NF-κB活性、骨桥蛋白mRNA表达明显下调。结论:血管紧张素Ⅱ诱导肾小管上皮细胞损伤与导致肾小管上皮细胞内NF-κB活性增加、骨桥蛋白mRNA转录上调有关。这一过程可能依赖血管紧张素ⅡⅠ型受体。

Angiotensin Ⅱ Induces the Injury of Proximal Tubular Cells

Objective To explore the mechanism of angiotensinⅡinducing the injury of proximal tubular cells.Methods Cultured cells were incubated with AngiotensinⅡ(10~(-7) μmol/l)as the control;cultured cells were incubated with different concentration Xiesartan for half an hour and then with angiotensinⅡ(10~(-7)μmol/l) as the intervention group;proximal tubular cells without stimulation as blank control;EMSA,RT-PCR were used to observe NF-κB activity and OPN mRNA expression in different periods,respectively.Results AngiotensinⅡcould increase NF-κB activity and upregulate OPN mRNA expression in proximal tubular cells.While Xiesartan could decrease NF-κB activity and downregulate OPN mRNA expression in angiotensinⅡ stimulated proximal tubular cells.Conclusion The mechanism of angiotensinⅡ inducing the injury of proximal tubular cells is related to increase NF-κB activity and upregulate OPN mRNA expression,and this process is angiotensinⅡ receptorⅠ dependent.