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首页> 外文期刊>Clinical journal of the American Society of Nephrology: CJASN >Indoxyl sulfate-induced endothelial dysfunction in patients with chronic kidney disease via an induction of oxidative stress
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Indoxyl sulfate-induced endothelial dysfunction in patients with chronic kidney disease via an induction of oxidative stress

机译：硫酸吲哚酚通过诱导氧化应激诱导的慢性肾脏病患者的内皮功能障碍

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Background and objectives: Recent data suggest indoxyl sulfate (IS), one of the uremic toxins that accelerate the progression of chronic kidney disease (CKD), may also be responsible for vascular disease via an induction of oxidative stress. The role of IS in endothelial dysfunction in CKD and potential mechanisms of IS-induced endothelial dysfunction were investigated. Design, setting, participants, & measurements: A prospective observational study in 40 CKD patients was performed. Flow-mediated endothelium-dependent vasodilatation (FMD) and its reaction time before and 24 weeks after an oral adsorbent of IS were evaluated. Plasma levels of IS and markers of oxidative stress were also measured. The proliferation, senescence, and production of nitric oxide and reactive oxygen species from human umbilical vein endothelial cells (HUVEC) were evaluated and the effect of antioxidants, N-acetylcysteine, rotenone, and apocynin was examined to explore the mechanism of IS-induced endothelial dysfunction. Results: AST-120 treatment for 24 weeks resulted in a significant increase in FMD with a decrease in IS and oxidized/reduced glutathione ratio. The presence of diabetes and high-sensitivity C-reactive protein were the independent predictors for an improved FMD. IS induced a production of reactive oxygen species in HUVEC, and pretreatment with antioxidants ameliorated IS-induced inhibition of proliferation and nitric oxide production and inhibited a senescence of HUVEC. Conclusions: IS may play an important role in endothelial dysfunction via generation of oxidative stress with an induction of endothelial senescence. AST-120 improved endothelial dysfunction in patients with CKD associated with a decrease in IS and a restoration of antioxidant reserve.
机译：背景与目的：最近的数据表明，吲哚酚硫酸盐（IS）是一种可促进慢性肾脏疾病（CKD）恶化的尿毒症毒素，也可能是通过诱发氧化应激而引起血管疾病的。研究了IS在CKD中内皮功能障碍中的作用以及IS诱导的内皮功能障碍的潜在机制。设计，设置，参与者和测量：对40名CKD患者进行了一项前瞻性观察研究。评估了IS口服吸附剂之前和之后24周的血流介导的内皮依赖性血管舒张（FMD）及其反应时间。还测量了血浆中的IS水平和氧化应激指标。评估了人脐静脉内皮细胞（HUVEC）的一氧化氮和活性氧的增殖，衰老和产生，并研究了抗氧化剂，N-乙酰半胱氨酸，鱼藤酮和载脂蛋白的作用，以探讨IS诱导的内皮细胞的机制。功能障碍。结果：AST-120治疗24周导致FMD显着增加，IS减少，谷胱甘肽氧化/降低。糖尿病和高敏C反应蛋白的存在是FMD改善的独立预测因素。 IS诱导了HUVEC中活性氧的产生，用抗氧化剂预处理可减轻IS诱导的增殖和一氧化氮生成的抑制，并抑制HUVEC的衰老。结论：IS可能通过产生氧化应激并诱导内皮衰老而在内皮功能障碍中发挥重要作用。 AST-120改善了CKD患者的血管内皮功能障碍，与IS减少和抗氧化剂储备的恢复有关。

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