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Agmatine attenuates silica-induced pulmonary fibrosis

机译：胍丁胺减轻二氧化硅诱发的肺纤维化

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There is a large body of evidence that nitric oxide (NO) formation is implicated in mediating silica-induced pulmonary fibrosis. As a reactive free radical, NO may not only contribute to lung parenchymal tissue injury but also has the ability to combine with superoxide and form a highly reactive toxic species peroxynitrite that can induce extensive cellular toxicity in the lung tissues. This study aimed to explore the effect of agmatine, a known NO synthase inhibitor, on silica-induced pulmonary fibrosis in rats. Male Sprague Dawley rats were treated with agmatine for 60 days following a single intranasal instillation of silica suspension (50 mg in 0.1 ml saline/rat). The results revealed that agmatine attenuated silica-induced lung inflammation as it decreased the lung wet/dry weight ratio, protein concentration, and the accumulation of the inflammatory cells in the bronchoalveolar lavage fluid. Agmatine showed antifibrotic activity as it decreased total hydroxyproline content of the lung and reduced silica-mediated lung inflammation and fibrosis in lung histopathological specimen. In addition, agmatine significantly increased superoxide dismutase (p < 0.001) and reduced glutathione (p < 0.05) activities with significant decrease in the lung malondialdehyde (p < 0.001) content as compared to the silica group. Agmatine also reduced silica-induced overproduction of pulmonary nitriteitrate as well as tumor necrosis factor ?±. Collectively, these results demonstrate the protective effects of agmatine against the silica-induced lung fibrosis that may be attributed to its ability to counteract the NO production, lipid peroxidation, and regulate cytokine effects.
机译：有大量证据表明，一氧化氮（NO）的形成与介导二氧化硅诱导的肺纤维化有关。作为反应性自由基，NO不仅可能导致肺实质组织损伤，而且还具有与超氧化物结合并形成高反应性有毒物种过氧亚硝酸盐的能力，该过氧亚硝酸盐可以在肺组织中引起广泛的细胞毒性。这项研究旨在探讨胍丁胺（一种已知的NO合酶抑制剂）对二氧化硅诱导的大鼠肺纤维化的影响。在鼻内滴注二氧化硅悬浮液（50 mg / 0.1 ml盐水/大鼠）后，用胍丁胺对雄性Sprague Dawley大鼠进行60天治疗。结果表明，胍丁胺减轻了二氧化硅引起的肺部炎症，因为它降低了肺湿/干重比，蛋白质浓度和支气管肺泡灌洗液中炎症细胞的积累。胍丁胺显示抗纤维化活性，因为它降低了肺组织病理学标本中的肺中总羟脯氨酸含量并减少了二氧化硅介导的肺部炎症和纤维化。此外，与硅胶组相比，胍丁胺显着增加了超氧化物歧化酶（p <0.001）和降低了谷胱甘肽（p <0.05）的活性，同时肺丙二醛的含量也明显降低（p <0.001）。胍丁胺还减少了二氧化硅诱导的肺亚硝酸盐/硝酸盐的过量生产以及肿瘤坏死因子α±。这些结果共同证明了胍丁胺对二氧化硅诱导的肺纤维化的保护作用，这可能归因于其抵抗NO生成，脂质过氧化和调节细胞因子作用的能力。

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