A novel glucosamine derivative exerts anti-inflammatory actions via inhibition of nuclear factor-kappaB

Jin A. Shin, Ji Sun Hwang, Song Yi Kim, Sei Kwan Oh, Ghilsoo Nam, Inn Oc Han

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Glucosamine suppresses lipopolysaccharide (LPS)-induced upregulation of pro-inflammatory mediators both in vivo and in culture systems of mouse microglia or macrophage. In the present study, we show that the novel glucosamine derivative, 2-deoxy-2-[(o-methylbenzylidene)]-β-glucopyranoside (NK-4), significantly reduced LPS-induced production of nitric oxide (NO) in BV2 microglia, RAW264.7 macrophage, and primary cultured peritoneal macrophages cells. NK-4 inhibited LPS-induced upregulation of inducible NO synthase (iNOS), cyclooxygenase-2, interleukin-6, tumor necrosis factor-α, and interleukin-1β in RAW264.7 cells in a time- and concentration-dependent manner. Furthermore, administering NK-4 significantly inhibited the induction of inflammatory cytokine mRNAs in the brains of LPS-injected mice. Although NK-4 inhibited LPS-induced nuclear factor-kappaB (NF-κB) activation, IκB-α degradation was not changed. Instead, NK-4 inhibited LPS-induced DNA-binding activity of NF-κB by suppressing p50 and c-Rel binding to NF-κB binding site of the iNOS promoter.

Original languageEnglish
Pages (from-to)162-167
Number of pages6
JournalNeuroscience Letters
StatePublished - 29 Aug 2013

Bibliographical note

Funding Information:
This work is supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) ( 2009-0073184 and 2010-0014338 ) and Inha University. There is no potential conflict of interest in this paper.


  • Glucosamine
  • NF-kappaB
  • NK-4


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