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鞣花酸通过调节四氯化碳诱导的大鼠 Nrf-2/NF-κB 信号通路预防肾损伤和氧化损伤。

Ellagic acid prevents kidney injury and oxidative damage via regulation of Nrf-2/NF-κB signaling in carbon tetrachloride induced rats.

机构信息

Faculty of Science, Department of Biology-Molecular Biology and Genetics Program, Firat University, Elazig, Turkey.

Faculty of Science, Department of Biology, Firat University, Elazig, Turkey.

出版信息

Mol Biol Rep. 2020 Oct;47(10):7959-7970. doi: 10.1007/s11033-020-05873-x. Epub 2020 Oct 2.

Abstract

Phytochemicals, bioactive food compounds, found in plants have been described as protective agents against renal injury. This work was planned to evaluate the effects of EA on anti-oxidative and anti-inflammation pathways in kidney damage induced with carbon tetrachloride. In this study, experimental animals (n = 36, 8 weeks old rats) were divided into 4 groups as follows: 1) Control group 2) EA group (10 mg/kg body weight) 3) CCl group (1.5 ml/kg, body weight) 4) EA + CCl group. The potentially protective effect of EA on kidney damage exposed by CCl in rats were evaluated. EA administration protects CCl induced kidney damage against oxidative stress through its antioxidant protection. Treatment of EA significantly reduced lipid peroxidation and improved glutathione and catalase enzyme activity. Recently studies showed that EA activated caspase-3 and nuclear transcription factor erythroid 2 related factor driven antioxidant signal pathway and protected the kidney against damage induced by oxidative stress. Furthermore, EA also markedly decreased the level of cyclooxygenase-2, the vascular endothelial growth factor and tumor necrosis factor-alpha and suppressed the protein synthesis of nuclear factor-kappa-B. This study reveals that EA has kidney protective effect against CCl induced oxidative damage and inflammation.

摘要

植物化学物质,生物活性食物化合物,存在于植物中,被描述为对抗肾损伤的保护剂。本工作旨在评估 EA 对四氯化碳诱导肾损伤的抗氧化和抗炎途径的影响。在这项研究中,实验动物(n=36,8 周龄大鼠)分为 4 组:1)对照组;2)EA 组(10mg/kg 体重);3)CCl 组(1.5ml/kg,体重);4)EA+CCl 组。评估 EA 对 CCl 暴露大鼠肾损伤的潜在保护作用。EA 给药通过其抗氧化保护作用,保护 CCl 诱导的肾损伤免受氧化应激。EA 治疗显著降低了脂质过氧化作用,改善了谷胱甘肽和过氧化氢酶的酶活性。最近的研究表明,EA 激活了半胱氨酸天冬氨酸蛋白酶-3 和核转录因子红细胞 2 相关因子驱动的抗氧化信号通路,保护肾脏免受氧化应激引起的损伤。此外,EA 还显著降低了环氧合酶-2、血管内皮生长因子和肿瘤坏死因子-α的水平,并抑制了核因子-κB 的蛋白质合成。本研究表明,EA 对 CCl 诱导的氧化损伤和炎症具有肾脏保护作用。

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