Sengul Emin, Gelen Volkan, Yildirim Serkan, Tekin Samet, Dag Yusuf
Department of Physiology, Faculty of Veterinary, Atatürk University, Erzurum, Turkey.
Department of Physiology, Faculty of Veterinary, Kafkas University, Kars, Turkey.
Biol Trace Elem Res. 2021 Jan;199(1):173-184. doi: 10.1007/s12011-020-02111-0. Epub 2020 Mar 12.
We sought to determine the effects of selenium (Se) on acrylamide (ACR)-induced nephrotoxicity in rats. In our study, 50 adult male Sprague-Dawley rats weighing 200-250 g were randomly divided into five groups. The control group was given intra-gastric (i.g.) saline (1 mL) for 10 days. The ACR group was given i.g. ACR in saline (38.27 mg/kg titrated to 1 mL) for 10 days. The Se0.5 + ACR and Se1 + ACR groups were administered Se in saline (0.5 and 1 mg/kg, respectively) for 10 days and given i.g. ACR (38.27 mg/kg) one hour after the Se injections. The Se1 group was administered i.g. Se (1 mg/kg) for 10 days. On day 11, intracardiac blood samples were obtained from the rats while they were under anesthesia, after which they were euthanized by decapitation. Urea and creatinine concentrations of blood serum samples were analyzed with an autoanalyzer. Enzyme-linked immunosorbence immunosorbent assay (ELISA) was used to quantify malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), tumor necrosis factor-α (TNF-α), nuclear factor-κB (NF-κB), interleukin (IL)-33, IL-6, IL-1β, cyclooxygenase-2 (COX-2), kidney injury molecule-1 (KIM-1), mitogen-activated protein kinase-1 (MAPK-1), and caspase-3 in kidney tissues. Renal tissues were evaluated by histopathological and immunohistochemical examinations for 8-hydroxylo-2'-deoxyguanosin 8-hydroxy-2'-deoxyguanosine (8-OhDG) and Bax. Serum urea and creatinine levels were higher in the ACR group than in the control, and these ACR-induced increases were prevented by high doses of Se. Additionally, ACR induced the renal oxidative stress, inflammation, apoptosis, and damage to DNA and tissue; likewise, these were prevented by high doses of Se. Taken with ACR, Se confers protection against ACR-induced nephrotoxicity in rats by reducing oxidative stress, inflammation, apoptosis, and DNA damage.
我们试图确定硒（Se）对丙烯酰胺（ACR）诱导的大鼠肾毒性的影响。在我们的研究中，将50只体重200 - 250克的成年雄性Sprague-Dawley大鼠随机分为五组。对照组给予胃内（i.g.）生理盐水（1毫升），持续10天。ACR组给予胃内注射生理盐水配制的ACR（38.27毫克/千克，定容至1毫升），持续10天。Se0.5 + ACR组和Se1 + ACR组分别给予胃内注射生理盐水配制的硒（分别为0.5和1毫克/千克），持续10天，并在注射硒1小时后给予胃内注射ACR（38.27毫克/千克）。Se1组给予胃内注射硒（1毫克/千克），持续10天。在第11天，在大鼠麻醉状态下采集心脏内血液样本，然后通过断头法使其安乐死。用自动分析仪分析血清样本中的尿素和肌酐浓度。采用酶联免疫吸附测定（ELISA）法对肾组织中的丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）、肿瘤坏死因子-α（TNF-α）、核因子-κB（NF-κB）、白细胞介素（IL）-33、IL-6、IL-1β、环氧化酶-2（COX-2）、肾损伤分子-1（KIM-1）、丝裂原活化蛋白激酶-1（MAPK-1）和半胱天冬酶-3进行定量分析。通过组织病理学和免疫组织化学检查评估肾组织中的8-羟基-2'-脱氧鸟苷（8-OhDG）和Bax。ACR组血清尿素和肌酐水平高于对照组，高剂量的硒可防止ACR诱导的这些升高。此外，ACR诱导了肾氧化应激、炎症、细胞凋亡以及DNA和组织损伤；同样，高剂量的硒可防止这些情况。与ACR一起使用时，硒通过降低氧化应激、炎症、细胞凋亡和DNA损伤，对ACR诱导的大鼠肾毒性具有保护作用。
