Heparin Attenuates the Expression of TNF alpha-induced Cerebral Endothelial Cell Adhesion Molecule

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Heparin is a well-known anticoagulant widely used in various clinical settings. Interestingly, recent studies have indicated that heparin also has anti-inflammatory effects on neuroinflammation-related diseases, such as Alzheimer's disease and meningitis. However, the underlying mechanism of its actions remains unclear. In the present study, we examined the anti-inflammatory mechanism of heparin in cultured cerebral endothelial cells (CECs), and found that heparin inhibited the tumor necrosis factor a (TNF alpha)-induced and nuclear factor kappa B (NF-kappa B)-dependent expression of adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), which are crucial for inflammatory responses. Heparin selectively interfered with NF-kappa B DNA-binding activity in the nucleus, which is stimulated by TNF alpha. In addition, non-anticoagulant 2,3-O desulfated heparin (ODS) prevented NF-kappa B activation by TNF alpha, suggesting that the anti-inflammatory mechanism of heparin action in CECs lies in heparin's ability to inhibit the expression of cell adhesion molecules, as opposed to its anticoagulant actions.
Publisher
KOREAN JOURNAL OF PHYSIOLOGY PHARMACOLOGY
Issue Date
2008-10
Language
English
Article Type
Article
Keywords

NF-KAPPA-B; BLOOD-BRAIN-BARRIER; LEUKOCYTE ADHESION; P-SELECTIN; INFLAMMATION; PHOSPHORYLATION; ACTIVATION; TRANSPORT; ARTHRITIS; CYTOKINES

Citation

KOREAN JOURNAL OF PHYSIOLOGY PHARMACOLOGY, v.12, no.5, pp.231 - 236

ISSN
1226-4512
URI
http://hdl.handle.net/10203/93184
Appears in Collection
MSE-Journal Papers(저널논문)
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