Ginsenoside Rg1 improves lipopolysaccharide-induced acute lung injury by inhibiting inflammatory responses and modulating infiltration of M2 macrophages
Ginsenoside Rg1 improves lipopolysaccharide-induced acute lung injury by inhibiting inflammatory responses and modulating infiltration of M2 macrophages
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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。
DOI：
10.1016/j.intimp.2015.06.022
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发表时间：
2015-09-01
影响因子：
5.6
通讯作者：
Li, Jinbao
中科院分区：
文献类型：
--
作者：
Bao, Suhong;Zou, Yun;Li, Jinbao
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特性。然而，人参皂苷 Rg1 对脂多糖 (LPS) 诱导的小鼠急性肺损伤 (ALI) 的影响尚不清楚。本研究旨在探讨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。所有小鼠在LPS给药前1小时腹腔内接受Rg1或等体积的磷酸盐缓冲盐水(PBS)。 LPS给药后6小时检测水肿定量、组织学和细胞凋亡。评估炎症细胞的数量、替代活化（M2）巨噬细胞的百分比以及支气管肺泡灌洗液（BALF）中的渗出物定量。测试了 caspase 3 的表达以及磷酸化 I kappa B-α 和 p65 的水平。结果显示，Rg1预处理组明显改善肺损伤，调节中性粒细胞和M2巨噬细胞的浸润，阻止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-kappa B 和 caspase 3 的激活。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，对 LPS 诱导的 ALI 发挥保护作用。 (C) 2015 年由 Elsevier B.V. 出版
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.