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首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Pu-erh black tea extract supplementation attenuates the oxidative DNA damage and oxidative stress in Sprague-Dawley rats with renal dysfunction induced by subchronic 3-methyl-2-quinoxalin benzenevinylketo-1,4-dioxide exposure
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Pu-erh black tea extract supplementation attenuates the oxidative DNA damage and oxidative stress in Sprague-Dawley rats with renal dysfunction induced by subchronic 3-methyl-2-quinoxalin benzenevinylketo-1,4-dioxide exposure

机译:补充普红茶提取物可减轻慢性亚甲基3-甲基-2-喹喔啉苯乙烯基酮-1,4-二氧化物暴露所致肾功能不全的Sprague-Dawley大鼠的氧化DNA损伤和氧化应激

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摘要

3-Methyl-2-quinoxalin benzenevinylketo-1,4-dioxide (Quinocetone, QCT), has been used to treat dysentery and promote growth in animal feeding. However, available data show that QCT has potential nephrotoxicity. The present study was designed to investigate the protective effects of Pu-erh black tea extract (PBTE) which is a traditional remedy in China with antioxidant properties against oxidative DNA damage and oxidative stress in a rat model of QCT-induced renal dysfunction. Increased serum creatinine, blood urea nitrogen, pathological lesions, urinary 8-hydroxy 2-deoxyguanosine (8-OHdG) and renal DNA damage were observed in the QCT-fed rats. These were accompanied by intracellular reactive oxygen species accumulation, enhanced lipid peroxidation, and inhibited antioxidant system, i.e., glutathione glutathione S-transferase, glutathione peroxidase and glutathione reductase. Oral administration of PBTE effectively suppressed QCT-induced renal dysfunction, as evidenced by reduced serum creatinine, urinary 8-OHdG and DNA damage in isolated renal cells, amelioration of oxidative stress and modulation of antioxidative system. In conclusion, PBTE administration ameliorated QCT-induced nephrotoxicity by maintaining DNA's double-helix architecture and mitigating oxidative stress.
机译:3-甲基-2-喹喔啉苯乙烯基酮-1,4-二氧化物(喹诺酮,QCT)已用于治疗痢疾并促进动物饲养中的生长。但是,现有数据表明QCT具有潜在的肾毒性。本研究旨在研究普-红茶提取物(PBTE)的保护作用,这是中国的传统药物,具有抗氧化DNA损伤和氧化应激的抗氧化特性,在QCT诱发的肾功能不全大鼠模型中。在QCT喂养的大鼠中观察到血清肌酐,血尿素氮增加,病理损害,尿中的8-羟基2-脱氧鸟苷(8-OHdG)和肾DNA损伤。这些伴随着细胞内活性氧的积累,增强的脂质过氧化作用和抑制的抗氧化剂系统,即谷胱甘肽谷胱甘肽S-转移酶,谷胱甘肽过氧化物酶和谷胱甘肽还原酶。口服PBTE可以有效抑制QCT诱导的肾功能不全,如血清肌酐减少,尿中的8-OHdG和分离的肾细胞中的DNA损伤,氧化应激的改善和抗氧化系统的调节所证明。总之,PBTE给药通过维持DNA的双螺旋结构和减轻氧化应激,改善了QCT诱导的肾毒性。

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