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目的:研究晚期糖基化终产物(AGES)修饰蛋白诱导人近端肾小管上皮HK-2细胞分泌纤溶酶原激活物抑制剂-1(PAI-1)的影响及其相关的氧化应激传导途径。方法:采用不同浓度AGES修饰的人血清白蛋白(AGES-HSA)与肾小管上皮HK-2细胞共培养。用光泽精化学发光法检测细胞匀浆中NADPH氧化酶活性,ELISA检测细胞上清液中PAI-1蛋白分泌,RT-PCR法检测PAI-1mRNA表达。结果:AGES-HSA诱导HK-2细胞NADPH氧化酶活化,并以时间、剂量依赖方式上调PAI-1蛋白和mRNA的表达。运用NADPH氧化酶抑制剂DPI、apocynin、氧自由基清除剂SOD可以明显阻断AG-ES-HSA诱导的PAI-1表达。结论:AGES-HSA可通过NADPH氧化酶依赖的氧化应激途径上调肾小管上皮细胞PAI-1表达。
AIM: To investigate the effects of advanced glycosylation end products (AGES) -mediated proteins on the secretion of plasminogen activator inhibitor-1 (PAI-1) from human proximal tubular epithelial cells HK-2 and its related oxidative stress Conduction pathway. Methods: AGES-modified human serum albumin (AGES-HSA) was co-cultured with HK-2 cells in renal tubular epithelial cells. The activity of NADPH oxidase in the cell homogenate was detected by lucigenin chemiluminescence. The PAI-1 protein secretion in the cell supernatant was detected by ELISA. The expression of PAI-1 mRNA was detected by RT-PCR. Results: AGES-HSA induced the activation of NADPH oxidase in HK-2 cells and up-regulated the expression of PAI-1 protein and mRNA in a time-and dose-dependent manner. Using NADPH oxidase inhibitor DPI, apocynin and oxygen free radical scavenger SOD could obviously block AG-ES-HSA-induced PAI-1 expression. Conclusion: AGES-HSA up-regulates the expression of PAI-1 in renal tubular epithelial cells through NADPH oxidase-dependent oxidative stress.