He Liyu, Peng Xiaofei, Zhu Jiefu, Liu Guoyong, Chen Xian, Tang Chengyuan, Liu Hong, Liu Fuyou, Peng Youming
Nephrology Department, 2nd Xiangya Hospital, Central South University, Key Lab of Kidney Disease and Blood Purification in Hunan, 139 Renmin Road, Changsha, Hunan 410011, People's Republic of China.
Can J Physiol Pharmacol. 2015 Apr;93(4):275-82. doi: 10.1139/cjpp-2014-0459. Epub 2015 Jan 20.
Gentamicin-induced nephrotoxicity is one of the most common causes of acute kidney injury (AKI). The phenotypic alterations that contribute to acute kidney injury include inflammatory response and oxidative stress. Curcumin has a wide range biological functions, especially as an antioxidant. This study was designed to evaluate the renoprotective effects of curcumin treatment in gentamicin-induced AKI.
Gentamicin-induced AKI was established in female Sprague-Dawley rats. Rats were treated with curcumin (100 mg/kg body mass) by intragastric administration, once daily, followed with an intraperitoneal injection of gentamicin sulfate solution at a dose of 80 mg/kg body mass for 8 consecutive days. At days 3 and 8, the rats were sacrificed, and the kidneys and blood samples were collected for further analysis.
The animals treated with gentamicin showed marked deterioration of renal function, together with higher levels of neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule 1 (KIM-1) in the plasma as compared with the controls. Animals that underwent intermittent treatment with curcumin exhibited significant improvements in renal functional parameters. We also observed that treatment with curcumin significantly attenuated renal tubular damage, apoptosis, and oxidative stress. Curcumin treatment exerted anti-apoptosis and anti-oxidative effects by up-regulating Nrf2/HO-1 and Sirt1 expression.
Our data clearly demonstrate that curcumin protects kidney from gentamicin-induced AKI via the amelioration of oxidative stress and apoptosis of renal tubular cells, thus providing hope for the amelioration of gentamicin-induced nephrotoxicity.
庆大霉素诱导的肾毒性是急性肾损伤（AKI）最常见的病因之一。导致急性肾损伤的表型改变包括炎症反应和氧化应激。姜黄素具有广泛的生物学功能，尤其是作为一种抗氧化剂。本研究旨在评估姜黄素治疗对庆大霉素诱导的急性肾损伤的肾脏保护作用。
在雌性Sprague-Dawley大鼠中建立庆大霉素诱导的急性肾损伤模型。大鼠通过灌胃给予姜黄素（100 mg/kg体重），每日一次，随后连续8天腹腔注射硫酸庆大霉素溶液，剂量为80 mg/kg体重。在第3天和第8天，处死大鼠，收集肾脏和血液样本进行进一步分析。
与对照组相比，接受庆大霉素治疗的动物肾功能显著恶化，血浆中中性粒细胞明胶酶相关脂质运载蛋白（NGAL）和肾损伤分子1（KIM-1）水平更高。接受姜黄素间歇治疗的动物肾功能参数有显著改善。我们还观察到，姜黄素治疗显著减轻了肾小管损伤、细胞凋亡和氧化应激。姜黄素治疗通过上调Nrf2/HO-1和Sirt1表达发挥抗凋亡和抗氧化作用。
我们的数据清楚地表明，姜黄素通过改善氧化应激和肾小管细胞凋亡保护肾脏免受庆大霉素诱导的急性肾损伤，从而为改善庆大霉素诱导的肾毒性带来希望。
