Correlation Engine 2.0
Clear Search sequence regions

  • ag490 (1)
  • CCL3 (6)
  • cells (2)
  • factor (3)
  • gene (1)
  • interleukin- 1β (4)
  • interleukin- 1β (2)
  • macrophages (4)
  • mice (1)
  • nAChR (4)
  • neuralgia (1)
  • pSTAT3 (3)
  • pyridines (2)
  • receptors (2)
  • signal (2)
  • STAT3 (3)
  • stat3 protein (1)
  • tc 2559 (6)
  • tyrphostins (2)
  • Sizes of these terms reflect their relevance to your search.

    The anti-inflammatory properties of TC-2559, an α4β2 nicotinic acetylcholine receptor (nAChR) agonist, on cultured murine macrophages was investigated. TC-2559 suppressed the upregulation of CC-chemokine ligand 3 (CCL3) and interleukin-1β (IL-1β) following lipopolysaccharide (LPS) treatment in J774A.1 cells. TC-2559 inhibited the phosphorylation of signal transducer and activator of transcription 3 (pSTAT3) but not nuclear factor-κB p65 after LPS. Blockade of pSTAT3 by AG490 inhibited the upregulation of CCL3 and IL-1β after LPS. In conclusion, TC-2559-driven α4β2 nAChR signaling suppressed the upregulation of CCL3 and IL-1β by inhibiting pSTAT3 in inflammatory macrophages, resulting in the suppression of neuropathic pain. Copyright © 2015 The Authors. Production and hosting by Elsevier B.V. All rights reserved.


    Norikazu Kiguchi, Fumihiro Saika, Yuka Kobayashi, Mei-Chuan Ko, Shiroh Kishioka. TC-2559, an α4β2 nicotinic acetylcholine receptor agonist, suppresses the expression of CCL3 and IL-1β through STAT3 inhibition in cultured murine macrophages. Journal of pharmacological sciences. 2015 Jun;128(2):83-6

    Expand section icon Mesh Tags

    Expand section icon Substances

    PMID: 26012743

    View Full Text