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首页> 外文期刊>International immunopharmacology >Protective effects of protocatechuic acid on acute lung injury induced by lipopolysaccharide in mice via p38MAPK and NF-kappa B signal pathways
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Protective effects of protocatechuic acid on acute lung injury induced by lipopolysaccharide in mice via p38MAPK and NF-kappa B signal pathways

机译：原儿茶酸通过p38MAPK和NF-κB信号通路对脂多糖诱导的小鼠急性肺损伤的保护作用

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摘要

The study aims to investigate the effects of protocatechuic acid (PCA) separated from Chinese herbs, on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. The mouse model was induced by intraperitoneal injection of LPS at the dose of 5 mg/kg body weight. Three doses of PCA (30, 15,5 mg/kg) were administered to mice with intraperitoneal injection one hour prior to LPS exposure. Six hours later after LPS administration, the effect of PCA on ALI mice was assessed via histopathological examination by HE staining, inflammatory cytokine production by ELISA assay and RT-PCR, p38MAPK and NF-kappa B activation by Western blot analysis. We found that PCA administration significantly ameliorated lung histopathological changes and decreased protein concentration in the bronchoalveolar lavage fluid. Furthermore, the overproduction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) was reduced by PCA. Additionally, PCA at the dose of 30 mg/kg could block the activation of p38MAPK and NF-kappa B signal pathways induced by LPS. In conclusion, our findings demonstrate that PCA possesses a protective effect on LPS-induced AU in mice via suppression of p38MAPK and NF-kappa B signal pathways. Therefore, PCA may be useful in the therapy of lung inflammatory diseases, especially for ALI. (c) 2015 Elsevier B.V. All rights reserved.
机译：这项研究旨在研究从中草药中分离出的原儿茶酸（PCA）对脂多糖（LPS）诱发的小鼠急性肺损伤（ALI）的影响。通过腹膜内注射剂量为5 mg / kg体重的LPS诱导小鼠模型。在LPS暴露前一小时，通过腹膜内注射向小鼠施用三剂PCA（30、15.5 mg / kg）。 LPS给药后六小时，通过HE染色的组织病理学检查，ELISA分析和RT-PCR的炎症细胞因子产生，Western blot分析的p38MAPK和NF-κB活化，评估PCA对ALI小鼠的作用。我们发现，PCA给药可显着改善肺组织病理学变化并降低支气管肺泡灌洗液中的蛋白质浓度。此外，PCA减少了肿瘤坏死因子-α（TNF-alpha）和白介素-1 beta（IL-1 beta）的过量生产。另外，剂量为30 mg / kg的PCA可以阻断LPS诱导的p38MAPK和NF-κB信号通路的激活。总之，我们的发现证明PCA通过抑制p38MAPK和NF-κB信号通路对LPS诱导的AU具有保护作用。因此，PCA在肺炎性疾病的治疗中可能是有用的，尤其是对于ALI。 （c）2015 Elsevier B.V.保留所有权利。

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