Heparin Attenuates the Expression of TNF alpha-induced Cerebral Endothelial Cell Adhesion Molecule
The Korean Journal of Physiology and Pharmacology
;
: 231-236, 2008.
Artigo
em Inglês
| WPRIM
| ID: wpr-728382
ABSTRACT
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 alpha(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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Heparina
/
Moléculas de Adesão Celular
/
NF-kappa B
/
Fator de Necrose Tumoral alfa
/
Molécula 1 de Adesão Intercelular
/
Molécula 1 de Adesão de Célula Vascular
/
Células Endoteliais
/
Doença de Alzheimer
/
Meningite
Idioma:
Inglês
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
2008
Tipo de documento:
Artigo
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