Heparin Attenuates the Expression of TNF<FONT FACE= HCI Tulip >Ձ-induced Cerebral Endothelial Cell Adhesion Molecule
Heparin Attenuates the Expression of TNF<FONT FACE= HCI Tulip >Ձ-induced Cerebral Endothelial Cell Adhesion Molecule
- Jeong Ho Lee Chul Hoon Kim Gi Ho Seo Jinu Lee Joo Hee Kim Dong Goo Kim Young Soo Ahn
- 대한생리학회-대한약리학회
- The Korean Journal of Physiology & Pharmacology
- 제12권 제5호
- 등재여부 : KCI등재
- 2008.01
- 231 - 236 (6 pages)
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 Ձ(TNFՁ)-induced and nuclear factor kappa B (NF-ՊB)-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-ՊB DNA-binding activity in the nucleus, which is stimulated by TNFՁ. In addition, non-anticoagulant 2,3-O desulfated heparin (ODS) prevented NF-ՊB activation by TNFՁ, 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.