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Glucosamine inhibits acute inflammatory mediator expression and neointima formation in balloon‐injured rat carotid artery
Author(s) -
Xing Dongqi,
Feng Wenguang,
Chen YiuFai,
HassanMajid Erum,
Chatham John C,
Oparil Suzanne
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a851-b
Subject(s) - neointima , proinflammatory cytokine , medicine , inflammation , artery , monocyte , ovariectomized rat , glucosamine , cell adhesion molecule , vasoprotective , endocrinology , restenosis , immunology , chemistry , stent , nitric oxide , biochemistry , estrogen
Background: It has been shown that increased levels of protein O‐linked‐N‐acetylglucosamine (O‐GlcNAc) increase cell survival following stress. This study tested whether increasing protein O‐GlcNAc levels with glucosamine (GlcN) inhibits acute inflammation and neointimal response to endoluminal injury of rat carotid artery. Methods and Results: Ovariectomized (OVX) rats randomly assigned to treatment with GlcN (0.3 mg/g BW/D, i.p.) or vehicle (V) were subjected to balloon injury of the right carotid artery. After 2 hrs and 14 days, rats were euthanized and both carotid arteries were processed for real‐time RT‐PCR (2 hrs) and morphometric analysis of neointimal thickening (14 days). At 2 hrs post injury, expression of mRNA for adhesion molecules (P‐selectin and vascular cell adhesion molecule‐1) and chemoattractants (cytokine‐induced neutrophil chemoattractant‐2β and monocyte chemoattractant protein‐1) were markedly increased in injured arteries of OVX+V rats. GlcN significantly attenuated expression of these proinflammatory mediators (by 30% to 50%). At 2 wks post injury, GlcN significantly reduced neointima formation in injured carotid arteries (by 60%). Conclusion: These results indicate that protein O‐GlcNAc in vasculature may represent a novel anti‐inflammatory and vasoprotective mechanism.