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

Title
Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury
Authors
Hwang S.-Y.Shin J.-H.Hwang J.-S.Kim S.-Y.Shin J.-A.Oh E.-S.Oh S.Kim J.-B.Lee J.-K.Han I.-O.
Ewha Authors
오억수오세관
SCOPUS Author ID
오억수scopus; 오세관scopus
Issue Date
2010
Journal Title
GLIA
ISSN
0894-1491JCR Link
Citation
vol. 58, no. 15, pp. 1881 - 1892
Indexed
SCI; SCIE; SCOPUS WOS scopus
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 antiinflammatory effects of GlcN were mainly attributable to its ability to inhibit nuclear factor kappaB (NF-jB) activation. GlcN inhibited LPS-induced nuclear translocation and DNA binding of p65 to both NF-jB consensus sequence and NF-jB 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. © 2010 Wiley-Liss, Inc.
DOI
10.1002/glia.21058
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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