Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury
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. N...
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| Veröffentlicht in: | Glia 2010-11, Vol.58 (15), p.1881-1892 |
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| creator | Hwang, So-Young Shin, Joo-Hyun Hwang, Ji-Sun Kim, Song-Yi Shin, Jin-A Oh, Eok-Soo Oh, Seikwan Kim, Jung-Bin Lee, Ja-Kyung Han, Inn-Oc |
| description | 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. © 2010 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/glia.21058 |
| format | Article |
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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. © 2010 Wiley‐Liss, Inc.</description><identifier>ISSN: 0894-1491</identifier><identifier>ISSN: 1098-1136</identifier><identifier>EISSN: 1098-1136</identifier><identifier>DOI: 10.1002/glia.21058</identifier><identifier>PMID: 20737476</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>amines ; Animals ; Antiinflammatory agents ; Brain ; Brain Infarction - drug therapy ; Brain Infarction - etiology ; Cell Line, Transformed ; Cell Survival - drug effects ; Cerebral blood flow ; Chimeras ; Chromatin Immunoprecipitation - methods ; Conserved sequence ; Disease Models, Animal ; Electrophoretic Mobility Shift Assay - methods ; Encephalitis - drug therapy ; Encephalitis - etiology ; Enzyme Inhibitors - pharmacology ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - genetics ; Glucosamine ; Glucosamine - therapeutic use ; Infarction, Middle Cerebral Artery - complications ; Inflammation ; Ischemia ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Macrophages ; Male ; Mice ; Microglia - drug effects ; Neurological diseases ; Neuroprotection ; Neuroprotective Agents - therapeutic use ; NF-kappa B - metabolism ; NF-kappaB ; Nitric-oxide synthase ; Nuclear transport ; Nucleotide sequence ; O-GlcNAcylation ; Promoters ; Rats ; Reperfusion ; RNA, Messenger - metabolism ; Severity of Illness Index ; Sugar ; Tetrazolium Salts ; Transfection - methods</subject><ispartof>Glia, 2010-11, Vol.58 (15), p.1881-1892</ispartof><rights>Copyright © 2010 Wiley‐Liss, Inc.</rights><rights>2010 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4988-c805601f4358f9ea4fe7d209729b7b0a0990b0f0410f319bdd2dda3f626da3bb3</citedby><cites>FETCH-LOGICAL-c4988-c805601f4358f9ea4fe7d209729b7b0a0990b0f0410f319bdd2dda3f626da3bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fglia.21058$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fglia.21058$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20737476$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hwang, So-Young</creatorcontrib><creatorcontrib>Shin, Joo-Hyun</creatorcontrib><creatorcontrib>Hwang, Ji-Sun</creatorcontrib><creatorcontrib>Kim, Song-Yi</creatorcontrib><creatorcontrib>Shin, Jin-A</creatorcontrib><creatorcontrib>Oh, Eok-Soo</creatorcontrib><creatorcontrib>Oh, Seikwan</creatorcontrib><creatorcontrib>Kim, Jung-Bin</creatorcontrib><creatorcontrib>Lee, Ja-Kyung</creatorcontrib><creatorcontrib>Han, Inn-Oc</creatorcontrib><title>Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury</title><title>Glia</title><addtitle>Glia</addtitle><description>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. © 2010 Wiley‐Liss, Inc.</description><subject>amines</subject><subject>Animals</subject><subject>Antiinflammatory agents</subject><subject>Brain</subject><subject>Brain Infarction - drug therapy</subject><subject>Brain Infarction - etiology</subject><subject>Cell Line, Transformed</subject><subject>Cell Survival - drug effects</subject><subject>Cerebral blood flow</subject><subject>Chimeras</subject><subject>Chromatin Immunoprecipitation - methods</subject><subject>Conserved sequence</subject><subject>Disease Models, Animal</subject><subject>Electrophoretic Mobility Shift Assay - methods</subject><subject>Encephalitis - drug therapy</subject><subject>Encephalitis - etiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - genetics</subject><subject>Glucosamine</subject><subject>Glucosamine - therapeutic use</subject><subject>Infarction, Middle Cerebral Artery - complications</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophages</subject><subject>Male</subject><subject>Mice</subject><subject>Microglia - drug effects</subject><subject>Neurological diseases</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>NF-kappa B - metabolism</subject><subject>NF-kappaB</subject><subject>Nitric-oxide synthase</subject><subject>Nuclear transport</subject><subject>Nucleotide sequence</subject><subject>O-GlcNAcylation</subject><subject>Promoters</subject><subject>Rats</subject><subject>Reperfusion</subject><subject>RNA, Messenger - metabolism</subject><subject>Severity of Illness Index</subject><subject>Sugar</subject><subject>Tetrazolium Salts</subject><subject>Transfection - methods</subject><issn>0894-1491</issn><issn>1098-1136</issn><issn>1098-1136</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EotvChR-AfERIaceOY8fHagXZSivgUOBoOckYXPKFnZTuv6-XtD3CaWbkZx6N9RLyhsE5A-AXPzpvzzmDonxGNgx0mTGWy-dkA6UWGROanZDTGG8AWBrUS3LCQeVKKLkhc9UtzRht7wekeIdhjtTSAZcwTmGcsZn9bXpwLnX01lsal2kKGKMfBzo66gfX2b6383H2Aw12pnWwqfOx-Ym9txcBJwxuiStxs4TDK_LC2S7i64d6Rr5-_HC93WX7z9XV9nKfNUKXZdaUUEhgTuRF6TRa4VC1HLTiulY1WNAaanAgGLic6bptedva3EkuU6nr_Iy8W73pK78XjLPp01XYdXbAcYmGqaLkQvJC_B8FprRUkquEvl_RJowxBnRmCr634ZAgcwzEHAMxfwNJ8NsH71L32D6hjwkkgK3AH9_h4R8qU-2vLh-l2brj44x3Tzs2_DIyaQvz_VNlvgHfVl92O3Od3wPJ9Kcg</recordid><startdate>20101115</startdate><enddate>20101115</enddate><creator>Hwang, So-Young</creator><creator>Shin, Joo-Hyun</creator><creator>Hwang, Ji-Sun</creator><creator>Kim, Song-Yi</creator><creator>Shin, Jin-A</creator><creator>Oh, Eok-Soo</creator><creator>Oh, Seikwan</creator><creator>Kim, Jung-Bin</creator><creator>Lee, Ja-Kyung</creator><creator>Han, Inn-Oc</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>20101115</creationdate><title>Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury</title><author>Hwang, So-Young ; Shin, Joo-Hyun ; Hwang, Ji-Sun ; Kim, Song-Yi ; Shin, Jin-A ; Oh, Eok-Soo ; Oh, Seikwan ; Kim, Jung-Bin ; Lee, Ja-Kyung ; Han, Inn-Oc</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4988-c805601f4358f9ea4fe7d209729b7b0a0990b0f0410f319bdd2dda3f626da3bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>amines</topic><topic>Animals</topic><topic>Antiinflammatory agents</topic><topic>Brain</topic><topic>Brain Infarction - drug therapy</topic><topic>Brain Infarction - etiology</topic><topic>Cell Line, Transformed</topic><topic>Cell Survival - drug effects</topic><topic>Cerebral blood flow</topic><topic>Chimeras</topic><topic>Chromatin Immunoprecipitation - methods</topic><topic>Conserved sequence</topic><topic>Disease Models, Animal</topic><topic>Electrophoretic Mobility Shift Assay - methods</topic><topic>Encephalitis - drug therapy</topic><topic>Encephalitis - etiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - genetics</topic><topic>Glucosamine</topic><topic>Glucosamine - therapeutic use</topic><topic>Infarction, Middle Cerebral Artery - complications</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophages</topic><topic>Male</topic><topic>Mice</topic><topic>Microglia - drug effects</topic><topic>Neurological diseases</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>NF-kappa B - metabolism</topic><topic>NF-kappaB</topic><topic>Nitric-oxide synthase</topic><topic>Nuclear transport</topic><topic>Nucleotide sequence</topic><topic>O-GlcNAcylation</topic><topic>Promoters</topic><topic>Rats</topic><topic>Reperfusion</topic><topic>RNA, Messenger - metabolism</topic><topic>Severity of Illness Index</topic><topic>Sugar</topic><topic>Tetrazolium Salts</topic><topic>Transfection - methods</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hwang, So-Young</creatorcontrib><creatorcontrib>Shin, Joo-Hyun</creatorcontrib><creatorcontrib>Hwang, Ji-Sun</creatorcontrib><creatorcontrib>Kim, Song-Yi</creatorcontrib><creatorcontrib>Shin, Jin-A</creatorcontrib><creatorcontrib>Oh, Eok-Soo</creatorcontrib><creatorcontrib>Oh, Seikwan</creatorcontrib><creatorcontrib>Kim, Jung-Bin</creatorcontrib><creatorcontrib>Lee, Ja-Kyung</creatorcontrib><creatorcontrib>Han, Inn-Oc</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Glia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hwang, So-Young</au><au>Shin, Joo-Hyun</au><au>Hwang, Ji-Sun</au><au>Kim, Song-Yi</au><au>Shin, Jin-A</au><au>Oh, Eok-Soo</au><au>Oh, Seikwan</au><au>Kim, Jung-Bin</au><au>Lee, Ja-Kyung</au><au>Han, Inn-Oc</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury</atitle><jtitle>Glia</jtitle><addtitle>Glia</addtitle><date>2010-11-15</date><risdate>2010</risdate><volume>58</volume><issue>15</issue><spage>1881</spage><epage>1892</epage><pages>1881-1892</pages><issn>0894-1491</issn><issn>1098-1136</issn><eissn>1098-1136</eissn><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. © 2010 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20737476</pmid><doi>10.1002/glia.21058</doi><tpages>12</tpages></addata></record> |
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| subjects | amines Animals Antiinflammatory agents Brain Brain Infarction - drug therapy Brain Infarction - etiology Cell Line, Transformed Cell Survival - drug effects Cerebral blood flow Chimeras Chromatin Immunoprecipitation - methods Conserved sequence Disease Models, Animal Electrophoretic Mobility Shift Assay - methods Encephalitis - drug therapy Encephalitis - etiology Enzyme Inhibitors - pharmacology Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Glucosamine Glucosamine - therapeutic use Infarction, Middle Cerebral Artery - complications Inflammation Ischemia Lipopolysaccharides Lipopolysaccharides - pharmacology Macrophages Male Mice Microglia - drug effects Neurological diseases Neuroprotection Neuroprotective Agents - therapeutic use NF-kappa B - metabolism NF-kappaB Nitric-oxide synthase Nuclear transport Nucleotide sequence O-GlcNAcylation Promoters Rats Reperfusion RNA, Messenger - metabolism Severity of Illness Index Sugar Tetrazolium Salts Transfection - methods |
| title | Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury |
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