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首页> 外文期刊>Jornal Brasileiro de Nefrologia >Priming prevent nephrotoxic acute renal failure through stimulation of antioxidant defense mechanism
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Priming prevent nephrotoxic acute renal failure through stimulation of antioxidant defense mechanism

机译：引发抗氧化剂防御机制可预防肾毒性急性肾衰竭

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Introduction: Priming is the mechanism of protection induced by a previous exposition of a cell or organ to low or equal concentrations of a toxic substance. Objective: To analyze the mechanism of priming induced by the previous exposition to gentamicin in human proximal tubular cells and nephrotoxic acute renal failure (ARF). Methods: Wistar rats and tubular cells were exposed to gentamicin 2mM during 24h or 40 mg/kg during 3 days and after one rest week were exposed to the same concentration during 24h in cells and additional ten days in rats. The primed animals were compared to control rats receiving vehicle and GENTA animals treated with the gentamicin during the same period. Biochemical parameters were analyzed. The oxidative stress was analyzed by urinary hydroperoxides and carbonylated protein while antioxidant defense was studied by antioxidant activity of the plasma (FRAP), catalase, superoxide dismutase, heme-oxygenase 1 (HO-1) immunostaining and enzymatic activity in kidney. Necrosis, apoptosis, proliferation, endothelin 1 (ET-1) and HO-1 expression were studied in cells. Results: Priming of the animals inhibited the increase in creatinine, urea, sodium excretion and urinary protein induced by gentamicin. Bosentan, ET-1 receptor antagonist, and hemin, HO-1 inducer, potentiate the inhibition. The mechanism of protection was mediated by induction of the antioxidant enzymes HO-1, catalase and SOD activity and oxidative stress reduction. Priming inhibited cell death and induced proliferation through ET-1 production. Conclusion: Priming is a persistent and multifactorial mechanism, the stimulation of the antioxidant defense could mimics partially the priming process and prevent the ARF.
机译：简介：启动是由先前将细胞或器官暴露于低浓度或相等浓度的有毒物质诱导的保护机制。目的：分析先前暴露于庆大霉素引起的人类近端肾小管细胞引发的引发和肾毒性急性肾衰竭（ARF）的机制。方法：Wistar大鼠和肾小管细胞在24h或40 mg / kg的环丙沙星中暴露3天，持续3h，并在24h内以相同的浓度暴露于大鼠中。将致敏动物与接受媒介物的对照大鼠和在同一时期用庆大霉素处理的GENTA动物进行比较。分析了生化参数。通过尿中的过氧化氢和羰基化蛋白分析了氧化应激，同时通过血浆的抗氧化活性（FRAP），过氧化氢酶，超氧化物歧化酶，血红素加氧酶1（HO-1）的免疫染色和肾脏的酶活性研究了抗氧化防御能力。研究了细胞中的坏死，凋亡，增殖，内皮素1（ET-1）和HO-1的表达。结果：引发动物抑制了庆大霉素诱导的肌酐，尿素，钠排泄和尿蛋白的增加。 ET-1受体拮抗剂Bosentan和HO-1诱导剂hemin增强了抑制作用。保护机制是通过诱导抗氧化酶HO-1，过氧化氢酶和SOD活性以及减少氧化应激来介导的。引发可抑制细胞死亡并通过ET-1产生诱导增殖。结论：引发是一个持久的多因素机制，抗氧化防御的刺激可以部分模拟引发过程并预防ARF。

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