Thymol Inhibits LPS-Stimulated Inflammatory Response via Down-Regulation of NF-κB and MAPK Signaling Pathways in Mouse Mammary Epithelial Cells

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• 作者：Dejie Liang (1)
  Fengyang Li (1)
  Yunhe Fu (1)
  Yongguo Cao (1)
  Xiaojing Song (1)
  Tiancheng Wang (1)
  Wei Wang (1)
  Mengyao Guo (1)
  Ershun Zhou (1)
  Depeng Li (1)
  Zhengtao Yang (1)
  Naisheng Zhang (1)
  
• 关键词：thymol ; lipopolysaccharide (LPS) ; mammary epithelial cells (MECs) ; nuclear factor ; kappaB (NF ; κB) ; mitogen ; activated protein kinases (MAPKs)
• 刊名：Inflammation
• 出版年：2014
• 出版时间：February 2014
• 年：2014
• 卷：37
• 期：1
• 页码：214-222
• 全文大小：332 KB
• 作者单位：Dejie Liang (1)
  Fengyang Li (1)
  Yunhe Fu (1)
  Yongguo Cao (1)
  Xiaojing Song (1)
  Tiancheng Wang (1)
  Wei Wang (1)
  Mengyao Guo (1)
  Ershun Zhou (1)
  Depeng Li (1)
  Zhengtao Yang (1)
  Naisheng Zhang (1)
  
  1. Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin Province, 130062, People’s Republic of China
  
• ISSN：1573-2576

文摘

Thymol is a natural monoterpene phenol primarily found in thyme, oregano, and tangerine peel. It has been shown to possess anti-inflammatory property both in vivo and in vitro. In the present paper, we studied the anti-inflammatory effect of thymol in lipopolysaccharide (LPS)-stimulated mouse mammary epithelial cells (mMECs). The mMECs were stimulated with LPS in the presence or absence of thymol (10, 20, 40?μg/mL). The concentrations of tumor necrosis factor α (TNF-α), interleukin (IL)-6, and IL-1β in the supernatants of culture were determined using enzyme-linked immunosorbent assay. Cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), nuclear factor-κB (NF-κB), and inhibitor protein of NF-κB (IκBα) were measured using western blot. The results showed that thymol markedly inhibited the production of TNF-α and IL-6 in LPS-stimulated mMECs. The expression of iNOS and COX-2 was also suppressed by thymol in a dose-dependent manner. Furthermore, thymol blocked the phosphorylation of IκBα, NF-κB p65, ERK, JNK, and p38 mitogen-activated protein kinases (MAPKs) in LPS-stimulated mMECs. These results indicate that thymol exerted anti-inflammatory property in LPS-stimulated mMECs by interfering the activation of NF-κB and MAPK signaling pathways. Thereby, thymol may be a potential therapeutic agent against mastitis.