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口服纳米银颗粒会在大鼠脑中独立于氧化应激激活犬尿氨酸途径。

The oral administration of silver nanoparticles activates the kynurenine pathway in rat brain independently of oxidative stress.

机构信息

Medicinal Biochemistry, Nanomedicine and Toxicology Laboratory, Department of Biochemistry, Landmark University, PMB 1001, Km 4, Ipetu Road, Omu-Aran, 251101, Nigeria.

Medicinal Biochemistry, Nanomedicine and Toxicology Laboratory, Department of Biochemistry, Landmark University, PMB 1001, Km 4, Ipetu Road, Omu-Aran, 251101, Nigeria.

出版信息

Chem Biol Interact. 2019 Apr 1;302:22-27. doi: 10.1016/j.cbi.2019.01.034. Epub 2019 Jan 29.

Abstract

In this work, we determined whether oxidative stress contributed to the activation of the kynurenine pathway by AgNPs. Male Wistar rats weighing between 130 and 146 g were randomly assigned into six groups. Animals in the negative control group were orally administered distilled water while, the other treatment groups were respectively given AgNPs (25 and 50 mg/kg bw) alone or in combination with Trolox (100 mg/kg bw). Results showed that treatments with AgNPs significantly raised protein carbonyl level in rat liver, but the co-treatment with Trolox attenuated the elevation. Conversely, AgNPs raised the level of reduced glutathione (GSH) in rat plasma and tissues compared to the negative control. Further, oral exposure to AgNPs (50 mg/kg bw) significantly elevated rat plasma and brain kynurenine levels compared to the negative control. Meantime, the co-treatment with Trolox appreciably restored kynurenine level in rat plasma, but not in the rat brain. Taken together, findings indicate that the oral administration of AgNPs alone at the doses used in this study, might not have caused oxidative stress. However, the co-treatment with Trolox appears to potentiate oxidative stress in rats following exposure to AgNPs. Furthermore, data support that the activation of the kynurenine pathway in the rat brain by AgNPs might be independent of oxidative stress. The findings are new and contribute to deepen our understanding of the cellular interaction by nanoparticles.

摘要

在这项工作中,我们确定了氧化应激是否导致 AgNPs 激活犬尿氨酸途径。体重在 130 至 146g 之间的雄性 Wistar 大鼠被随机分为六组。阴性对照组动物经口给予蒸馏水,而其他处理组分别给予 AgNPs(25 和 50mg/kg bw)单独或与 Trolox(100mg/kg bw)联合处理。结果表明,AgNPs 处理显著提高了大鼠肝脏中的蛋白质羰基水平,但 Trolox 的共同处理减轻了这种升高。相反,与阴性对照组相比,AgNPs 提高了大鼠血浆和组织中的还原型谷胱甘肽(GSH)水平。此外,与阴性对照组相比,口服暴露于 50mg/kg bw 的 AgNPs 显著提高了大鼠血浆和大脑中的犬尿氨酸水平。同时,Trolox 的共同处理显著恢复了大鼠血浆中的犬尿氨酸水平,但对大鼠大脑中的犬尿氨酸水平没有影响。总之,这些发现表明,在本研究中使用的剂量下,单独口服 AgNPs 可能不会引起氧化应激。然而,与 Trolox 的共同处理似乎会增强大鼠暴露于 AgNPs 后的氧化应激。此外,数据支持 AgNPs 激活大鼠大脑中的犬尿氨酸途径可能与氧化应激无关。这些发现是新的,有助于加深我们对纳米颗粒细胞相互作用的理解。

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