Oxidative Stress in Animal Models of Acute and Chronic Renal Failure

Oxidative Stress in Animal Models of Acute and Chronic Renal Failure
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DOI:
10.1155/2019/8690805
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发表时间:
2019-01-01
期刊:
影响因子:
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通讯作者:
Tothova, Lubomira
Tothova, Lubomira
中科院分区:
医学4区
文献类型:
--
作者:
Gyuraszova, Marianna;Kovalcikova, Alexandra Gaal;Tothova, Lubomira

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导论.肾脏疾病是一种全球性的健康和经济负担,患病率不断上升。需要寻找生物标志物,以便更早和更有效地进行疾病筛查和监测。氧化应激与急性肾损伤(阿基)和慢性肾病(CKD)有关。我们研究的目的是调查氧化应激和抗氧化状态的全身标志物的浓度是否受到阿基和CKD的影响,并确定潜在的生物标志物。方法.在成年雄性Wistar大鼠中,通过双侧肾切除诱导阿基,并且通过5/6肾切除诱导CKD。阿基患者在手术后48小时和CKD患者在手术后6个月采集血液。测定晚期氧化蛋白产物(AOPP)、硫代巴比妥酸反应物质(TBARS)、晚期糖基化终产物(AGEs)、果糖胺、总抗氧化能力(TAC)和铁还原抗氧化能力(FRAP)。结果阿基和CKD动物的高浓度血浆肌酐和尿素证实了肾功能受损。与相应的对照组相比,阿基中的AOPP和果糖胺分别高出100%和54%,CKD中的AOPP和果糖胺分别高出100%和199%。同样,阿基期间AGEs(92%)和TAC(102%)增加了约两倍。在CKD中,作为抗氧化状态标志物的FRAP浓度与对照组相比增加了一倍(107%),但另一种抗氧化状态标志物TAC的浓度在两组之间没有差异。结论.阿基和CKD导致全身氧化应激增加。AOPP和果糖胺可以被认为是急性和慢性肾损伤的潜在生物标志物。另一方面,AGEs,TAC和FRAP似乎是疾病特异性的,这可能有助于区分急性和慢性肾损伤。然而,这需要在临床研究中进一步验证。
Introduction. Kidney disease is a worldwide health and economic burden, with rising prevalence. The search for biomarkers for earlier and more effective disease screening and monitoring is needed. Oxidative stress has been linked to both, acute kidney injury (AKI) and chronic kidney disease (CKD). The aim of our study was to investigate whether the concentrations of systemic markers of oxidative stress and antioxidant status are affected by AKI and CKD, and to identify potential biomarkers. Methods. In adult male Wistar rats, AKI was induced by bilateral nephrectomy, and CKD was induced by 5/6 nephrectomy. Blood was collected 48 hours after surgery in AKI and 6 months after surgery in CKD. Advanced oxidation protein products (AOPP), thiobarbituric acid reactive substances (TBARS), advanced glycation end products (AGEs), fructosamine, total antioxidant capacity (TAC), and ferric reducing antioxidant power (FRAP) were measured. Results. Impaired renal function was confirmed by high concentrations of plasma creatinine and urea in AKI and CKD animals. AOPP and fructosamine were higher by 100% and 54% in AKI, respectively, and by 100% and 199% in CKD, respectively, when compared to corresponding control groups. Similarly, there was approximately a twofold increase in AGEs (by 92%) and TAC (by 102%) during AKI. In CKD, concentrations of FRAP, as an antioxidative status marker, were doubled (by 107%) when compared to the control group, but concentration of TAC, another marker of antioxidative status, did not differ between the groups. Conclusions. AKI and CKD led to increased systemic oxidative stress. AOPP and fructosamine could be considered potential biomarkers for both, acute and chronic kidney damage. On the other hand, AGEs, TAC, and FRAP seem to be disease specific, which could help to differentiate between acute and chronic kidney injuries. However, this needs further validation in clinical studies.