Cytoprotection of Perfluorocarbon on PMVECs In Vitro

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• 作者：Shufeng Xu (1) (2)
  Ping Wang (1)
  Kun Wei (2)
  Fengsui Liu (2)
  Zhixin Liang (1)
  Xiaowei Zhao (1)
  Aimin Li (3)
  Liangan Chen (1)
  
• 关键词：perfluorocarbon ; lipopolysaccharide ; TLR ; 4 ; NF ; κB ; pulmonary vascular endothelial cells
• 刊名：Inflammation
• 出版年：2013
• 出版时间：April 2013
• 年：2013
• 卷：36
• 期：2
• 页码：512-520
• 全文大小：578KB
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• 作者单位：Shufeng Xu (1) (2)
  Ping Wang (1)
  Kun Wei (2)
  Fengsui Liu (2)
  Zhixin Liang (1)
  Xiaowei Zhao (1)
  Aimin Li (3)
  Liangan Chen (1)
  
  1. Department of Pulmonary Medicine, Chinese People’s Liberation Army General Hospital, Beijing, 100853, People’s Republic of China
  2. Department of Respiratory Medicine, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, 066000, China
  3. Department of Respiratory Medicine, The First Hospital of Shanxi Medical University, Taiyuan, Shanxi, 030001, China
  
• ISSN：1573-2576

文摘

Lipopolysaccharide (LPS) can activate endothelial cells and induce inflammatory injury. Toll-like receptor-4 (TLR-4) is integrally involved in LPS signaling and has a requisite role in the activation of nuclear factor (NF)-κB. A number of studies have demonstrated the cytoprotective action of perfluorocarbon (PFC) both in vivo and in vitro, but the exact mechanisms have yet to be elucidated. In this study, we examined in an in vitro model the cytoprotective effect of PFC on LPS-stimulated pulmonary vascular endothelial cells (PMVECs). Intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), and interleukin-8 (IL-8) were significantly increased in the LPS-stimulated PMVECs groups. The expression of TLR-4 mRNA and protein in LPS groups was markedly increased. Meanwhile, NF-κB was activated. There were no significant effects of PFC alone on any of the factors studied while the coculture group showed significant downregulation of the secretion of ICAM-1, TNF-α, and IL-8; the expression of TLR-4 mRNA; and the activity of NF-κB. LPS can induce PMVEC inflammatory injury via the activation of TLR-4 and subsequent activation of NF-κB. PFC is able to protect PMVECs from LPS-induced inflammatory injury by blocking the initiation of the LPS signaling pathway.