Daidzein attenuates lipopolysaccharide-induced acute lung injury via toll-like receptor 4/NF-kappaB pathway

被引:99
作者
Feng, Guang [1 ,2 ]
Sun, Bo [4 ]
Li, Tian-zuo [1 ,3 ]
机构
[1] Capital Med Univ, Beijing Tongren Hosp, Dept Anesthesiol, Beijing 100730, Peoples R China
[2] Xuzhou Med Coll, Dept Anesthesiol, Affiliated Hosp, Xuzhou 221002, Peoples R China
[3] Capital Med Univ, Beijing Shijitan Hosp, Dept Anesthesiol, Beijing 100038, Peoples R China
[4] Soochow Univ, Dept Anesthesiol, Affiliated Hosp 2, Suzhou 215004, Peoples R China
基金
中国国家自然科学基金;
关键词
Acute lung injury; Acute respiratory distress syndrome; Daidzein; Lipopolysaccharide; Toll-like receptor 4; NF-kappaB; RESPIRATORY-DISTRESS-SYNDROME; NF-KAPPA-B; SOY ISOFLAVONES; CELLS; PATHOGENESIS; INFLAMMATION; ACTIVATION; EXPRESSION; GENISTEIN; MACROPHAGES;
D O I
10.1016/j.intimp.2015.04.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
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.
引用
收藏
页码:392 / 400
页数:9
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