Fisetin Alleviates Lipopolysaccharide-Induced Acute Lung Injury via TLR4-Mediated NF-κB Signaling Pathway in Rats

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• 作者：Guang Feng ; Ze-yu Jiang ; Bo Sun ; Jie Fu ; Tian-zuo Li
• 关键词：acute lung injury ; acute respiratory distress syndrome ; fisetin ; lipopolysaccharide ; Toll ; like receptor 4 ; NF ; κB
• 刊名：Inflammation
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：39
• 期：1
• 页码：148-157
• 全文大小：981 KB
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• 作者单位：Guang Feng (1)
  Ze-yu Jiang (3)
  Bo Sun (4)
  Jie Fu (3)
  Tian-zuo Li (2)
  
  1. Department of Anesthesiology, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, 221002, People’s Republic of China
  3. Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou, 221002, People’s Republic of China
  4. Department of Anesthesiology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, People’s Republic of China
  2. Department of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, People’s Republic of China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Rheumatology
  Internal Medicine
  Pharmacology and Toxicology
  Pathology
  
• 出版者：Springer Netherlands
• ISSN：1573-2576

文摘

Acute lung injury (ALI), a common component of systemic inflammatory disease, is a life-threatening condition without many effective treatments. Fisetin, a natural flavonoid from fruits and vegetables, was reported to have wide pharmacological properties such as anti-inflammatory, antioxidant, and anticancer activities. The aim of this study was to detect the effects of fisetin on lipopolysaccharide (LPS)-induced acute lung injury and investigate the potential mechanism. Fisetin was injected (1, 2, and 4 mg/kg, i.v.) 30 min before LPS administration (5 mg/kg, i.v.). Our results showed that fisetin effectively reduced the inflammatory cytokine release and total protein in bronchoalveolar lavage fluids (BALF), decreased the lung wet/dry ratios, and obviously improved the pulmonary histology in LPS-induced ALI. Furthermore, fisetin inhibited LPS-induced increases of neutrophils and macrophage infiltration and attenuated MPO activity in lung tissues. Additionally, fisetin could significantly inhibit the Toll-like receptor 4 (TLR4) expression and the activation of NF-κB in lung tissues. Our data indicates that fisetin has a protective effect against LPS-induced ALI via suppression of TLR4-mediated NF-κB signaling pathways, and fisetin may be a promising candidate for LPS-induced ALI treatment. KEY WORDS acute lung injury acute respiratory distress syndrome fisetin lipopolysaccharide Toll-like receptor 4 NF-κB