Cornuside Suppresses Lipopolysaccharide-Induced Inflammatory Mediators by Inhibiting Nuclear Factor-Kappa B Activation in RAW 264.7 Macrophages

  • Choi Yun Ho
    Department of Anatomy, Medical School, Institute for Medical Sciences, Chonbuk National University
  • Jin Guang Yu
    Yanbian University Hospital, Medicine College, Yanbian University
  • Li Guang Zhao
    Department of Anatomy and Histology and Embryology, School of Basic Medical Sciences, Yanbian University
  • Yan Guang Hai
    Department of Anatomy and Histology and Embryology, School of Basic Medical Sciences, Yanbian University

この論文をさがす

抄録

Cornuside, a secoiridoid glucoside compound, was isolated from the fruit of Cornus officinalis SIEB. et ZUCC. Cornuside has been reported to possess immunomodulatory and anti-inflammatory activities. However, the effects and mechanism of action of cornuside in inflammation have not been fully characterized. The present study was therefore designed to examine whether cornuside suppresses inflammatory response in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Cornuside significantly inhibited the LPS-induced production of nitric oxide, prostaglandin E2, tumor necrosis factor-alpha, interleukin-6 (IL-6), and IL-1beta. The mRNA and protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were also decreased by cornuside. Furthermore, cornuside significantly attenuated the LPS-stimulated phosphorylation and degradation of inhibitory kappa B-alpha and the subsequent translocation of the p65 subunit of nuclear factor-kappa B (NF-κB) to the nucleus. Cornuside also reduced the phosphorylations of extracellular-signal-related kinase (ERK1/2), p38, and c-Jun N-terminal kinase (JNK1/2). These results suggest that the anti-inflammatory property of cornuside is related to the downregulations of iNOS and COX-2 due to NF-κB inhibition as well as the negative regulation of ERK1/2, p38, and JNK1/2 phosphorylations in RAW 264.7 cells.

収録刊行物

被引用文献 (2)*注記

もっと見る

参考文献 (34)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ