<scp><i>O</i></scp>‐<scp>GlcNA</scp>cylation and p50/p105 binding of c‐<scp>R</scp>el are dynamically regulated by <scp>LPS</scp> and glucosamine in <scp>BV</scp>2 microglia cells

Abstract

In BV2 microglial cells, the anti-inflammatory effect of GlcN is mediated by prevention of the prolonged activation of transcription factors, c-Rel and NF-κB. Further clarification of the mechanism by which GlcN exerts this effect will facilitate the development of pharmacological strategies for preventing excessive NO formation when targeting inflammatory diseases of the periphery or CNS.