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Methanolic bark extract of Acacia catechu ameliorates benzo(a) pyrene induced lung toxicity by abrogation of oxidative stress, inflammation, and apoptosis in mice

机译:儿茶金合欢的甲醇树皮提取物可消除小鼠的氧化应激,炎症和细胞凋亡,从而改善苯并(a)induced诱导的肺毒性

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摘要

Benzo(a)pyrene [B(a)P] is a well-known carcinogen present in the environment In this study, we evaluated the protective potential of methanolic bark extract of Acacia catechu Willd. (MEBA) against the lung toxicity induced by B(a)P in Swiss albino mice. To determine the protective efficacy of MEBA, it was orally administered to the mice at two doses (200 and 400 mg/kg body weight) once daily for 7 days. Mice were also exposed (orally) to B(a)P at a dose of 125 mg/kg body weight on 7th day. Administration of B(a)P increased the activities of toxicity markers such as LDH, LPO, and XO with a subsequent decrease in the activities of tissue anti-oxidant armory (CAT, SOD, GST, GPx, GR, QR, and GSH). It also caused activation of the apoptotic and inflammatory pathway by upregulation of TNF-α, NF-kB, COX-2, p53, bax, caspase-3, and downregulating Bcl-2. Pretreatment with MEBA at two different doses (200 and 400 mg/kg body weight) significantly ameliorates B(a)P-induced increased toxicity markers and activities of detoxifying enzymes along with the levels of glutathione content. It also significantly attenuated expression of apoptotic and inflammatory markers in the lungs. Histological results further confirmed the protective role of MEBA against B(a)P-induced lung toxicity. The results indicate that MEBA may be beneficial in ameliorating the B(a)P-induced oxidative stress, inflammation, and apoptosis in the lungs of mice.
机译:苯并(a)[[B(a)P]是存在于环境中的一种著名的致癌物。在这项研究中,我们评估了金合欢(Acacia catechu Willd)的甲醇树皮提取物的保护潜力。 (MEBA)对抗瑞士白化病小鼠中B(a)P诱导的肺毒性。为了确定MEBA的保护功效,每天两次以两次剂量(200和400 mg / kg体重)对小鼠口服给予,共7天。在第7天,还将小鼠口服(口服)B(a)P,剂量为125 mg / kg体重。 B(a)P的使用增加了LDH,LPO和XO等毒性标志物的活性,随后组织抗氧化武器库(CAT,SOD,GST,GPx,GR,QR和GSH)的活性降低。它还通过上调TNF-α,NF-kB,COX-2,p53,bax,caspase-3和下调Bcl-2引起凋亡和炎性途径的激活。用MEBA进行两种不同剂量(200和400 mg / kg体重)的预处理可显着改善B(a)P诱导的毒性标志物和排毒酶活性以及谷胱甘肽含量水平的增加。它还显着减弱了肺中凋亡和炎性标志物的表达。组织学结果进一步证实了MEBA对B(a)P诱导的肺毒性的保护作用。结果表明,MEBA可能有助于改善B(a)P诱导的小鼠肺部的氧化应激,炎症和细胞凋亡。

著录项

  • 来源
    《Environmental toxicology》 |2017年第6期|1566-1577|共12页
  • 作者单位

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

    Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India;

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  • 正文语种 eng
  • 中图分类
  • 关键词

    lung toxicity; bcl-2; apoptosis; antioxidants; histopathology;

    机译:肺毒性;bcl-2;细胞凋亡抗氧化剂;组织病理学;

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