Department of Histology and Embryology, Faculty of Medicine, Trakya University, Edirne, Turkey.
Iran J Kidney Dis. 2022 Mar;16(2):96-107.
The antioxidant activity of curcumin (CMN) has been evaluated in several studies. We aimed to examine the protective effect of curcumin on gentamicin-induced nephrotoxicity in rats, both at histological and immunohistochemical levels.
Forty male Wistar albino rats were assigned into four groups of 10 as follows: group 1: control, group 2: curcumin for 15 days, group 3: gentamicin for the last 10 days, and group 4: curcumin for 15 days and gentamicin for the last 10 days. Curcumin (100 mg/kg/d) was gavaged, and gentamicin (80 mg/kg/d) was injected intraperitoneally. Kidney tissues and blood were collected for histological, immunohistochemical and biochemical studies. Body weight and kidney weight/body weight changes were recorded.
Gentamicin nephrotoxicity was characterized by a significant rise in serum urea and creatinine levels and a significant reduction in body weight and an increase in kidney weight/body weight. The gentamicin group showed degenerative changes in tubules and glomeruli together with, increased phosphorylated (p)-p38 mitogen-activated protein kinase (p38 MAPK) positive cells in immunohistochemical evaluation, increased immunoreactivity of nuclear factor-kappa B (NFkB), and decreased immunoreactivity of nuclear factor erythroid 2-related factor 2 (Nrf2). Curcumin diminished body weight loss caused by gentamicin administration but, did not change the kidney weight/body weight. Moreover, curcumin ameliorated the histological alterations and reduced the biochemical parameters. Additionaly, curcumin significantly decreased p-p38 MAPK positive cells and NFkB immunoreactivity, while significantly increasing Nrf2 immunoreactivity in the kidney tissue.
We conclude that curcumin may attenuate gentamicininduced nephrotoxicity by supprresing the p38 MAPK and NFkB, and activating the Nrf2 signaling pathways. DOI: 10.52547/ijkd.6647.
姜黄素（CMN）的抗氧化活性已在多项研究中得到评估。我们旨在研究姜黄素对大鼠庆大霉素诱导的肾毒性的保护作用，从组织学和免疫组织化学水平进行研究。
将 40 只雄性 Wistar 白化大鼠分为 4 组，每组 10 只：第 1 组：对照组；第 2 组：姜黄素治疗 15 天；第 3 组：庆大霉素治疗 10 天；第 4 组：姜黄素治疗 15 天，庆大霉素治疗 10 天。姜黄素（100mg/kg/d）灌胃，庆大霉素（80mg/kg/d）腹腔注射。收集肾脏组织和血液进行组织学、免疫组织化学和生化研究。记录体重和肾脏重量/体重变化。
庆大霉素肾毒性的特征是血清尿素和肌酐水平显著升高，体重显著减轻，肾脏重量/体重增加。免疫组织化学评价显示，庆大霉素组肾小管和肾小球出现退行性变化，磷酸化（p）-p38 丝裂原活化蛋白激酶（p38MAPK）阳性细胞增加，核因子-kappa B（NFkB）免疫反应性增加，核因子红细胞 2 相关因子 2（Nrf2）免疫反应性降低。姜黄素减少了庆大霉素引起的体重减轻，但没有改变肾脏重量/体重。此外，姜黄素改善了组织学改变，降低了生化参数。此外，姜黄素显著减少了肾脏组织中 p-p38MAPK 阳性细胞和 NFkB 免疫反应性，同时显著增加了 Nrf2 免疫反应性。
我们得出结论，姜黄素可能通过抑制 p38MAPK 和 NFkB 并激活 Nrf2 信号通路来减轻庆大霉素诱导的肾毒性。DOI：10.52547/ijkd.6647.
