分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

Protective effect of Cistanche deserticola on gentamicin-induced nephrotoxicity in rats

Ruibin Bai, Jingmin Fan, Yanping Wang, Yan Wang, Xue Li, Fangdi Hu

Journal:Chinese Herbal Medicines

IF:0

DOI:10.1016/j.chmed.2022.03.008

PMID:36875447

Published:2022-12-16

research field:毒理学药理学植物疗法肾病学

Abstract

Objective Gentamicin (GM) is a commonly used aminoglycoside antibiotic, however, renal toxicity has limited its usage. The present study was designed to evaluate the ameliorative effect of Cistanche deserticola on GM-induced nephrotoxicity in rats. Methods The nephrotoxicity in rats was induced by intraperitoneal administration of GM (100 mg/kg) for 10 consecutive days. Glomerular filtration rate, blood urea nitrogen, creatinine and kidney histopathology were detected to assess the GM-induced nephrotoxicity. The oxidative stress (catalase, superoxide dismutase, glutathione and malondialdehyde) was assessed. The inflammatory response (tumor necrosis factor-α, interleukin-6, myeloperoxidase and nuclear factor-kappa B) and apoptotic marker (Bax and Bcl-2) were also evaluated. Results The results showed that water and 75% ethanol extracts of C. deserticola (named CDW and CDE, respectively) (100, 200 and 400 mg/kg) in combination with GM could recover the reduction of glomerular filtration rate and enhance the renal endogenous antioxidant capability induced by GM. The increase in the expression of renal inflammatory cytokines (tumor necrosis factor-α and interleukin-6), nuclear protein of nuclear factor-kappa B (p65) and the activity of myeloperoxidase induced by GM was significantly decreased upon CDW or CDE treatment. In addition, CDW or CDE treatment could decrease the Bax protein expression and increase the Bcl-2 protein expression in GM-induced nephrotoxicity in rats significantly. Conclusion The study demonstrated that C. deserticola treatment could attenuate kidney dysfunction and structural damage in rats induced by GM through the reduction of inflammation, oxidative stress and apoptosis.

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