Department of Pathology, School of Medicine, Mustafa Kemal University, Hatay, Turkey.
Ren Fail. 2012;34(8):991-7. doi: 10.3109/0886022X.2012.706880.
Radiocontrast-induced nephropathy has become one of the most important causes of renal acute failure. The most effective management of reducing the incidence of contrast nephropathy is to understand and prevent its causes. We aimed to investigate the protective role of ebselen against radiocontrast-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats.
Albino Wistar rats were randomly separated into four groups. The Group 1 rats were treated with sodium chloride as the control group, Group 2 with radiocontrast, Group 3 with radiocontrast plus ebselen, and Group 4 with ebselen alone. After 24 h, the animals over the experimental period were euthanized and blood samples were analyzed for blood urea nitrogen (BUN) and serum creatinine (Cr) levels. Kidney sections were analyzed for malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as histopathological changes.
In the radiocontrast group, BUN, MDA, and GSH-Px levels increased while SOD activity decreased compared with the control group. These decays were improved by ebselen administration in the radiocontrast group. Significant histological deteriorations were observed in the radiocontrast group. We noted improvement in the histologic findings with ebselen administration.
These results indicate that ebselen might produce a protective mechanism against radiocontrast-induced nephrotoxicity.
造影剂肾病已成为急性肾衰竭的重要原因之一。降低造影剂肾病发生率的最有效方法是了解和预防其病因。我们旨在研究依布硒啉在大鼠组织氧化剂/抗氧化剂参数和光镜方面对放射造影剂诱导的肾毒性的保护作用。
白化 Wistar 大鼠随机分为四组。第 1 组大鼠用氯化钠作为对照组，第 2 组用造影剂，第 3 组用造影剂加依布硒啉，第 4 组用依布硒啉。24 h 后，实验组的动物被安乐死，分析血液样本的血尿素氮（BUN）和血清肌酐（Cr）水平。分析肾脏切片中的丙二醛（MDA）水平以及超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-Px）的活性以及组织病理学变化。
与对照组相比，造影剂组的 BUN、MDA 和 GSH-Px 水平升高，SOD 活性降低。依布硒啉在造影剂组中的给药改善了这些衰减。在造影剂组中观察到明显的组织学恶化。我们注意到依布硒啉给药可改善组织学发现。
这些结果表明，依布硒啉可能对放射造影剂诱导的肾毒性产生保护机制。
