These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Modulation of TNF-alpha-induced endothelial cell activation by glucosamine, a naturally occurring amino monosaccharide.
    Author: Ju Y, Hua J, Sakamoto K, Ogawa H, Nagaoka I.
    Journal: Int J Mol Med; 2008 Dec; 22(6):809-15. PubMed ID: 19020780.
    Abstract:
    Atherosclerosis is now considered a chronic inflammatory disease, and glucosamine has the potential to exhibit an anti-inflammatory action. Thus, we investigated the effect of glucosamine on tumor necrosis factor alpha (TNF-alpha)-induced endothelial cell activation. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNF-alpha in the presence or absence of glucosamine or its analogue, N-acetylglucosamine. mRNA expression of MCP-1 (a chemoattractant protein) and ICAM-1 (an adhesion molecule) was evaluated by real-time RT-PCR, and their protein levels were analyzed by ELISA and Western blotting, respectively. Furthermore, the effects of glucosamine on the phosphorylation of p38MAPK and NF-kappaB, and O-N-acetylglucosamine (O-GlcNAc) modification were evaluated by Western blotting. The results demonstrated that glucosamine but not N-acetylglucosamine suppressed TNF-alpha-induced expression of MCP-1 and ICAM-1 at both the mRNA and protein levels. Furthermore, glucosamine abrogated the phosphorylation of p38MAPK and NF-kappaB. To note, glucosamine induced O-GlcNAc modification, which was negatively correlated with the expression of MCP-1 and ICAM-1, and phosphorylation of p38MAPK and NF-kappaB. Thus, glucosamine is likely to suppress endothelial cell activation (TNF-alpha-induced ICAM-1 and MCP-1 expression) possibly by affecting p38MAPK and NF-kappaB signaling via O-GlcNAc modification.
    [Abstract] [Full Text] [Related] [New Search]