Astragalin attenuates lipopolysaccharide-induced inflammatory responses by down-regulating NF-κB signaling pathway

Astragalin attenuates lipopolysaccharide-induced inflammatory responses by down-regulating NF-κB signaling pathway
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DOI:
10.1016/j.bbrc.2012.02.005
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发表时间:
2012-03-09
影响因子:
3.1
通讯作者:
Deng, Xuming
Deng, Xuming
中科院分区:
生物学4区
文献类型:
--
作者:
Soromou, Lanan Wassy;Chen, Na;Deng, Xuming

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黄芪甲苷 (AG) 是一种来自许多传统草药和药用植物的黄酮类化合物,据描述具有体外抗炎活性。本研究旨在确定黄芪甲苷对脂多糖诱导的小鼠内毒素血症和肺损伤的保护作用及其潜在机制。给小鼠腹膜内(i.p.)注射脂多糖(LPS)(剂量范围:540 mg/kg)。我们观察小鼠的死亡率,连续 7 天,每天两次,并记录存活率。在药物测试中,我们通过在 LPS 攻击前 1 小时口服黄芪甲苷来检查黄芪甲素(25、50 或 75 mg/kg)对 LPS 诱导的内毒素血症的治疗效果。使用 LPS 诱导的急性肺损伤 (ALI) 实验模型,我们检查了黄芪甲苷在解决肺损伤中的作用。研究表明,在脂多糖诱导的急性肺损伤小鼠模型中,黄芪甲苷预处理可以提高致命性内毒素血症期间的生存率并减轻炎症反应。黄芪发挥抗炎作用的机制与通过灭活 NF-κ B 来抑制肿瘤坏死因子-a (TNF-α)、白介素-1 (IL-1) 和白细胞介素-6 (IL-6) 的产生相关。 (C) 2012 Elsevier Inc. 保留所有权利。
Astragalin (AG), a flavonoid from many traditional herbs and medicinal plants, has been described to exhibit in vitro anti-inflammatory activity. The present study aimed to determine the protective effects and the underlying mechanisms of astragalin on lipopolysaccharide-induced endotoxemia and lung injury in mice. Mice were injected intraperitoneally (i.p.) with lipopolysaccharide (LPS) (dose range: 540 mg/kg). We observed mice on mortality for 7 days twice a day and recorded survival rates. In drug testing, we examined the therapeutic effects of astragalin (25, 50 or 75 mg/kg) on LPS-induced endotoxemia by dosing orally astragalin 1 hour before LPS challenge. Using an experimental model of LPS-induced acute lung injury (ALI), we examined the effect of astragalin in resolving lung injury. The investigations revealed that pretreatment with astragalin can improve survival during lethal endotoxemia and attenuate inflammatory responses in a murine model of lipopolysaccharide-induced acute lung injury. The mechanisms by which Astragalin exerts its anti-inflammatory effect are correlated with inhibition of tumor necrosis factor-a (TNF-alpha), interleukin-1 (IL-1), and interleukin-6 (IL-6) production via inactivation of NF-kappa B. (C) 2012 Elsevier Inc. All rights reserved.