We investigated whether thymoquinone (TQ) exerts a beneficial effect on renal injury due to amikacin (AK) administration in rats. To generate kidney damage with AK, a single 1.2 g/kg dose of AK was administered intraperitoneally. TQ was administered orally to the AK treated group at a dose of 40 mg/kg for five days. At the end of the experiment, rats were sacrificed and blood samples were used to measure blood urea nitrogen (BUN) and creatinine (Cr) levels. Kidney samples were taken to measure the oxidative stress biomarker, malondialdehyde (MDA), and expression of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT). Because reactive oxygen species (ROS) and apoptosis contribute to tissue damage associated with NADPH oxidase (NOX), we also investigated NOX-2, NOX-4 and apoptosis marker, caspase-3, expression using immunohistochemistry. MDA, BUN, Cr, NOX-2, NOX-4 and caspase-3 production were increased, and SOD and CAT were decreased in the AK treated group compared to controls. MDA, BUN, Cr, NOX-2, NOX-4 and caspase-3 levels were decreased, and SOD and CAT levels were increased in TQ + AK treated rats compared to AK treated animals. TQ appears to protect the kidney from the toxic effects of AK.

中文翻译：

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胸腺醌对阿米卡星的保护可引起大鼠肾损伤。

我们调查了胸腺醌（TQ）是否对大鼠因丁胺卡那霉素（AK）给药而对肾脏损伤产生了有益的影响。为了用AK引起肾脏损害，腹膜内施用1.2 g / kg剂量的AK。将TQ以40 mg / kg的剂量口服给予AK治疗组，持续5天。实验结束时，处死大鼠，并使用血液样本测量血尿素氮（BUN）和肌酐（Cr）的水平。采集肾脏样品以测量氧化应激生物标志物，丙二醛（MDA）以及抗氧化酶，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的表达。由于活性氧（ROS）和凋亡会导致与NADPH氧化酶（NOX）相关的组织损伤，因此我们还研究了NOX-2，NOX-4和凋亡标记物caspase-3，表达使用免疫组织化学。与对照组相比，AK处理组的MDA，BUN，Cr，NOX-2，NOX-4，caspase-3产量增加，SOD和CAT降低。与AK处理的动物相比，TQ + AK处理的大鼠MDA，BUN，Cr，NOX-2，NOX-4和caspase-3的水平降低，而SOD和CAT的水平升高。TQ似乎可以保护肾脏免受AK的毒性作用。