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首页> 外文期刊>International immunopharmacology >Ginsenoside Rg1 improves lipopolysaccharide-induced acute lung injury by inhibiting inflammatory responses and modulating infiltration of M2 macrophages
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Ginsenoside Rg1 improves lipopolysaccharide-induced acute lung injury by inhibiting inflammatory responses and modulating infiltration of M2 macrophages

机译:人参皂苷Rg1通过抑制炎症反应和调节M2巨噬细胞的浸润来改善脂多糖诱导的急性肺损伤

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Ginsenoside Rg1 (Rg1), the major effective component of ginseng, has been reported to have potent antiinflammatory properties. However, the effect of ginsenoside Rg1 on lipopolysaccharide (LPS) -induced acute lung injury (ALI) in mice was unknown. The present study was designed to investigate the protective role of Rg1 on LPS-induced ALI and explore the potential mechanisms. The mice were divided randomly into four groups: the sham group, the LPS group and the LPS + Rg1 (40 mg/kg or 200 mg/kg) pretreatment groups. All mice received Rg1 or an equivalent volume of phosphate buffer saline (PBS) intraperitoneally 1 h before LPS administration. Edema quantification, histology, and apoptosis were detected 6 h after LPS administration. The number of inflammatory cells, the percentage of alternative activated (M2) macrophages and the exudate quantification in bronchoalveolar lavage fluid (BALF) were evaluated. The caspase 3 expression, and the levels of phosphorylated I kappa B-alpha and p65 were tested. The results showed that the Rg1 pretreatment group markedly improved lung damage, modulated the infiltration of neutrophils and M2 macrophages, prevented the production of protein and proinflammatory cytokines in BALF, and inhibited apoptosis in lung. We also found that Rg1 suppressed NF-kappa B and caspase 3 activation. These data suggest that Rg1 plays a protective role against LPS-induced ALI by ameliorating inflammatory responses, regulating the infiltration of M2 macrophages, and inhibiting pulmonary cell apoptosis. (C) 2015 Published by Elsevier B.V.
机译:人参皂苷Rg1(Rg1)是人参的主要有效成分,据报道具有有效的抗炎作用。但是,人参皂苷Rg1对脂多糖(LPS)诱导的小鼠急性肺损伤(ALI)的作用尚不清楚。本研究旨在调查Rg1对LPS诱导的ALI的保护作用,并探讨其潜在机制。将小鼠随机分为四组:假手术组,LPS组和LPS + Rg1(40mg / kg或200mg / kg)预处理组。在给予LPS之前1小时,所有小鼠腹膜内接受Rg1或等体积的磷酸盐缓冲盐水(PBS)。 LPS给药后6小时检测到水肿定量,组织学和凋亡。评估炎症细胞的数量,替代活化的(M2)巨噬细胞的百分比以及支气管肺泡灌洗液(BALF)中的渗出液定量。测试了胱天蛋白酶3的表达以及磷酸化的IκB-α和p65的水平。结果表明,Rg1预处理组可显着改善肺损伤,调节中性粒细胞和M2巨噬细胞的浸润,防止BALF中蛋白质和促炎细胞因子的产生,并抑制肺细胞凋亡。我们还发现Rg1抑制NF-κB和caspase 3激活。这些数据表明,Rg1通过改善炎症反应,调节M2巨噬细胞的浸润和抑制肺细胞凋亡而对LPS诱导的ALI起到保护作用。 (C)2015由Elsevier B.V.发布

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