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芦丁通过抗氧化和抗炎活性改善硫酸铜诱导的大鼠脑损伤。

Rutin ameliorates copper sulfate-induced brain damage via antioxidative and anti-inflammatory activities in rats.

作者信息

Arowoogun Jeremiah, Akanni Olubukola O, Adefisan Adedoyin O, Owumi Solomon E, Tijani Abiola S, Adaramoye Oluwatosin A

机构信息

Department of Biochemistry, Drug Metabolism and Toxicology Research Laboratories, University of Ibadan, Ibadan, Nigeria.

Department of Biochemistry, Cancer Research and Molecular Biology Laboratories, University of Ibadan, Ibadan, Nigeria.

出版信息

J Biochem Mol Toxicol. 2021 Jan;35(1):e22623. doi: 10.1002/jbt.22623. Epub 2020 Sep 2.

DOI:10.1002/jbt.22623
PMID:32881150
Abstract

Excessive exposure to Copper (Cu) may result in Cu toxicity and adversely affect health outcomes. We investigated the protective role of rutin on Cu-induced brain damage. Experimental rats were treated as follows: group I: control; group II: Cu-sulfate: 200 mg/kg; group III: Cu-sulfate, and rutin 100 mg/kg; and group IV: rutin 100 mg/kg, for 7 weeks. Cu only treatment significantly decreased body weight gain, while rutin cotreatment reversed this decrease. Cu treatment increased malondialdehyde, nitric oxide level, and myeloperoxidase activity and decreased superoxide dismutase and catalase activities in rat brain. Immunohistochemistry showed that COX-2, iNOS, and Bcl-2 proteins were strongly expressed, while Bax was mildly expressed in the brain of Cu-treated rats. Furthermore, brain histology revealed degenerated neurons, and perforated laminae of cerebral cortex in the Cu-only treated rats. Interestingly, coadministration of Cu and rutin reduced the observed histological alteration, improved inflammatory and antioxidant biomarkers, thereby protecting against Cu-induced brain damage via antioxidative and anti-inflammatory mechanisms.

摘要

过量接触铜(Cu)可能导致铜中毒,并对健康结果产生不利影响。我们研究了芦丁对铜诱导的脑损伤的保护作用。实验大鼠的处理如下:第一组:对照组;第二组:硫酸铜:200毫克/千克;第三组:硫酸铜加100毫克/千克芦丁;第四组:100毫克/千克芦丁,持续7周。仅硫酸铜处理显著降低了体重增加,而芦丁联合处理逆转了这种下降。硫酸铜处理增加了大鼠脑中丙二醛、一氧化氮水平和髓过氧化物酶活性,并降低了超氧化物歧化酶和过氧化氢酶活性。免疫组织化学显示,环氧化酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)和Bcl-2蛋白在硫酸铜处理的大鼠脑中强烈表达,而Bax轻度表达。此外,脑组织学显示仅硫酸铜处理的大鼠中神经元退化,大脑皮质板层穿孔。有趣的是,铜和芦丁联合给药减少了观察到的组织学改变,改善了炎症和抗氧化生物标志物,从而通过抗氧化和抗炎机制预防铜诱导的脑损伤。

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