Protective effects of genistein in homocysteine-induced endothelial cell inflammatory injury

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• 作者：Shengbo Han (1)
  Hui Wu (2)
  Wenxue Li (3)
  Pan Gao (1)
  
  1. Clinical Laboratory of Zhengzhou Traditional Chinese Medicine Hospital ; Wenhuagong Road 65 ; Zhengzhou ; 450007 ; China
  2. School of Public Health ; Xinxiang Medical University ; East of JinSui Road of XinXiang City ; Xinxiang ; 453003 ; Henan ; China
  3. Clinical Laboratory of The Eighth People鈥檚 Hospital of Zhengzhou City ; Ruimin street ; Zhengzhou ; 450006 ; China
  
• 关键词：Cytokine ; Genistein ; Homocysteine ; Inflammatory injury ; ROS
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2015
• 出版时间：May 2015
• 年：2015
• 卷：403
• 期：1-2
• 页码：43-49
• 全文大小：691 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

Hyperhomocysteinemia is a risk factor for cardiovascular disease and the mechanism of homocysteine (HCY)-induced vascular endothelial cell injury has been intensively studied for many years. Recently, a large number of studies have shown inhibitory effects of genistein (GEN), a soy isoflavone, in the process of endothelial cell injury. In the present study, the protective effects of GEN in HCY-induced endothelial cell inflammatory injury were investigated. A model of HCY-induced endothelial cell (ECV-304) inflammatory injury was established in vitro, and the protective effect of GEN in this procession was explored. According to our results, GEN protected HCY-induced endothelial cell from viability decreases, meanwhile prevented the changes of cell morphology and the production of reactive oxygen species (ROS). The expression of NF-kB P-65, IL-6, and ICAM-1 was all down-regulated. During the HCY-induced endothelial cell injury, the endothelial cell apoptosis and proliferation disorder were alleviated. Therefore, we conclude that HCY-induced endothelial cell inflammatory injury could be blocked by GEN. The present findings suggest that GEN protects HCY-induced endothelial cell inflammatory injury may through reducing the release of ROS, inhibiting NF-kB activation, down-regulating the expression of cytokine IL-6 and adhesion molecules ICAM-1, avoiding inflammatory cells and platelet adhesion, accordingly, leading to a balance of endothelial cell proliferation and apoptosis.