Bai Ruibin, Fan Jingmin, Wang Yanping, Wang Yan, Li Xue, Hu Fangdi
State Key Laboratory of Functional Organic Molecular Chemistry, Institute of Codonopsis Radix, School of Pharmacy, Lanzhou University, Lanzhou 730000, China.
Codonopsis Radix Research Institute, Lanzhou 730000, China.
Chin Herb Med. 2022 Dec 16;15(1):102-109. doi: 10.1016/j.chmed.2022.03.008. eCollection 2023 Jan.
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 on GM-induced nephrotoxicity in rats.
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.
The results showed that water and 75% ethanol extracts of (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.
The study demonstrated that treatment could attenuate kidney dysfunction and structural damage in rats induced by GM through the reduction of inflammation, oxidative stress and apoptosis.
庆大霉素（GM）是一种常用的氨基糖苷类抗生素，然而，肾毒性限制了其使用。本研究旨在评估[具体物质]对GM诱导的大鼠肾毒性的改善作用。
通过连续10天腹腔注射GM（100mg/kg）诱导大鼠肾毒性。检测肾小球滤过率、血尿素氮、肌酐和肾脏组织病理学以评估GM诱导的肾毒性。评估氧化应激（过氧化氢酶、超氧化物歧化酶、谷胱甘肽和丙二醛）。还评估炎症反应（肿瘤坏死因子-α、白细胞介素-6、髓过氧化物酶和核因子-κB）和凋亡标志物（Bax和Bcl-2）。
结果表明，[具体物质]的水提取物和75%乙醇提取物（分别命名为CDW和CDE）（100、200和400mg/kg）与GM联合使用可恢复肾小球滤过率的降低，并增强GM诱导的肾脏内源性抗氧化能力。CDW或CDE处理后，GM诱导的肾脏炎症细胞因子（肿瘤坏死因子-α和白细胞介素-6）表达增加、核因子-κB（p65）核蛋白表达增加以及髓过氧化物酶活性增加均显著降低。此外，CDW或CDE处理可显著降低GM诱导的大鼠肾毒性中Bax蛋白表达并增加Bcl-2蛋白表达。
该研究表明，[具体物质]处理可通过减轻炎症、氧化应激和凋亡来减轻GM诱导的大鼠肾功能障碍和结构损伤。
