Daidzein attenuates lipopolysaccharide-induced acute lung injury via toll-like receptor 4/NF-kappaB pathway
Daidzein attenuates lipopolysaccharide-induced acute lung injury via toll-like receptor 4/NF-kappaB pathway
复制标题
大豆黄酮通过 Toll 样受体 4/NF-kappaB 途径减轻脂多糖诱导的急性肺损伤。
DOI：
10.1016/j.intimp.2015.04.002
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发表时间：
2015-06-01
影响因子：
5.6
通讯作者：
Li, Tian-zuo
中科院分区：
文献类型：
--
作者：
Feng, Guang;Sun, Bo;Li, Tian-zuo
大豆黄酮是一种从许多植物和草药中提取的多酚类化合物，据报道具有抗炎作用。然而，大豆黄酮对脂多糖（LPS）诱导的急性肺损伤的影响尚未确定。本研究旨在观察大豆黄酮对内毒素诱导的急性肺损伤的影响，并探讨其分子机制。大鼠腹腔注射LPS（5 mg/kg）后30 min腹腔注射大豆黄酮（2、4、8 mg/kg）。结果表明，大豆黄酮组肺组织学改变明显，肺湿/干重比值明显降低。我们还发现，大豆黄酮显着抑制LPS诱导的肺组织巨噬细胞和中性粒细胞浸润的增加，以及显着减弱MPO活性。此外，大豆黄酮还能有效地降低支气管肺泡灌洗液（BALF）中炎性细胞因子的释放和总蛋白。此外，大豆苷元显着抑制LPS诱导的肺组织中Toll样受体4（TLR 4）和骨髓分化因子88（MyD 88）蛋白的上调表达以及NF-κ B的活化。体外实验中，大豆黄酮可明显抑制LPS刺激的A549肺泡上皮细胞TLR 4和MyD 88的表达及NF-κ B B的活化。总之，这些数据表明大豆黄酮对LPS诱导的ALI的抗炎作用可能是由于其抑制TLR 4-MyD 88-NF-κ B通路的能力，大豆黄酮可能是LPS诱导的ALL的潜在治疗剂（C）2015 Elsevier B. V.版权所有。
Daidzein, a diphenolic isoflavone from many plants and herbs, has been reported to have anti-inflammatory properties. However, the effects of daidzein on lipopolysaccharide (LPS)-induced acute lung injury have not been determined. The aim of this study was to detect the effects of daidzein on LPS-induced acute lung injury and investigate the molecular mechanisms. Daidzein was intraperitoneally injected (2, 4, 8 mg/kg) 30 min after intratracheal instillation of LPS (5 mg/kg) in rats. The results showed that daidzein treatment remarkably improved the pulmonary histology and decreased the lung wet/dry weight ratios. We also found that daidzein significantly inhibited LPS-induced increases of macrophages and neutrophils infiltration of lung tissues, as well as markedly attenuated MPO activity. Moreover, daidzein effectively reduced the inflammatory cytokines release and total protein in bronchoalveolar lavage fluids (BALF). Furthermore, daidzein significantly inhibited LPS-induced toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) protein up-expressions and NF-kappa B activation in lung tissues. In vitro, daidzein obviously inhibited the expressions of TLR4 and MyD88 and the activation of NF-kappa B in LPS-stimulated A549 alveolar epithelial cells. In conclusion, these data indicate that the anti-inflammatory effects of daidzein against LPS-induced ALI may be due to its ability to inhibit TLR4-MyD88-NF-kappa B pathway and daidzein may be a potential therapeutic agent for LPS-induced ALL (C) 2015 Elsevier B.V. All rights reserved.