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. 2010 Nov 15;58(15):1881-92.
doi: 10.1002/glia.21058.

Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury

So-Young Hwang  1 , Joo-Hyun Shin, Ji-Sun Hwang, Song-Yi Kim, Jin-A Shin, Eok-Soo Oh, Seikwan Oh, Jung-Bin Kim, Ja-Kyung Lee, Inn-Oc Han
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Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury

So-Young Hwang et al. Glia. .

Erratum in

Abstract

We investigated the neuroprotective effect of glucosamine (GlcN) in a rat middle cerebral artery occlusion model. At the highest dose used, intraperitoneal GlcN reduced infarct volume to 14.3% ± 7.4% that of untreated controls and afforded a reduction in motor impairment and neurological deficits. Neuroprotective effects were not reproduced by other amine sugars or acetylated-GlcN, and GlcN suppressed postischemic microglial activation. Moreover, GlcN suppressed lipopolysaccharide (LPS)-induced upregulation of proinflammatory mediators both in vivo and in culture systems using microglial or macrophage cells. The anti-inflammatory effects of GlcN were mainly attributable to its ability to inhibit nuclear factor kappaB (NF-κB) activation. GlcN inhibited LPS-induced nuclear translocation and DNA binding of p65 to both NF-κB consensus sequence and NF-κB binding sequence of inducible nitric oxide synthase promoter. In addition, we found that GlcN strongly repressed p65 transactivation in BV2 cells using Gal4-p65 chimeras system. P65 displayed increased O-GlcNAcylation in response to LPS; this effect was also reversed by GlcN. The LPS-induced increase in p65 O-GlcNAcylation was paralleled by an increase in interaction with O-GlcNAc transferase, which was reversed by GlcN. Finally, our results suggest that GlcN or its derivatives may serve as novel neuroprotective or anti-inflammatory agents.

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