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KMID : 0811720080120050231
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Korean Journal of Physiology & Pharmacology
2008 Volume.12 No. 5 p.231 ~ p.236
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Heparin Attenuates the Expression of TNFα-induced Cerebral Endothelial Cell Adhesion Molecule
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Lee Jeong-Ho
Ahn Young-Soo
Kim Dong-Goo
Kim Chul-Hoon
Seo Gi-Ho
Lee Jinu
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Abstract
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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 ?(TNF?)-induced and nuclear factor kappa B (NF-?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-?B DNA-binding activity in the nucleus, which is stimulated by TNF?. In addition, non-anticoagulant 2,3-O desulfated heparin (ODS) prevented NF-?B activation by TNF?, 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.
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KEYWORD
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Heparin, NF-κB, ICAM-1, VCAM-1, Cerebral endothelial cells, Anti-inflammation
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