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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。
Objective: To investigate the mechanism of angiotensin Ⅱ-induced renal tubular epithelial cell injury. Methods: Angiotensin Ⅱ (10-7μmol / l) was added to renal tubular epithelial cells as control group; cultured tubular epithelial cells served as blank control; different concentrations of valsartan (10-6μmol / l, 10-7μmol / l , 10-8μmol / l, 10-9μmol / l) and tubular epithelial cells co-cultured for half an hour before adding angiotensin Ⅱ (10-7μmol / l) for the intervention group; EMSA, RT- NF-κB activity, osteopontin mRNA expression. Results: Angiotensin Ⅱ induced an increase in NF-κB activity and osteopontin mRNA expression in renal tubular epithelial cells. However, valsartan intervention group showed that NF-κB activity and osteopontin mRNA expression were significantly down-regulated. CONCLUSION: Angiotensin II-induced tubular epithelial cell injury is associated with an increase of NF-κB activity and up-regulation of osteopontin mRNA in renal tubular epithelial cells. This process may depend on angiotensin Ⅱ type Ⅰ receptor.