[摘要] 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(10-7 μmol/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(10-6 μmol/l、10-7 μmol/l、10-8 μmol/l、10-9 μmol/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(10-7 μmol/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。

    [关键词] 血管紧张素Ⅱ;肾小管上皮细胞;核转录因子-κB;骨桥蛋白

    AngiotensinⅡInduces the Injury of Proximal Tubular Cells

    ZHANG Jian-e, LUO Chang-xia, ZHANG Qing-hong, LI Tao

    (Department of Nephrology, Taihe Hospital, Yunyang Medical College, Shiyan, Hubei 442000,China)

    Abstract： 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(10-7μmol/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. ......