title: Heparin Attenuates the Expression of TNFalpha-induced Cerebral Endothelial Cell Adhesion Molecule.
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(TNFalpha)-induced and nuclear factor kappa B (NF-kappaB)-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-kappaB DNA-binding activity in the nucleus, which is stimulated by TNFalpha. In addition, non-anticoagulant 2,3-O desulfated heparin (ODS) prevented NF-kappaB activation by TNFalpha, 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.
authors: Department of Pharmacology, Brain Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, Korea.
authors: Jeong Ho
authors: JH
authors: Lee
authors: Chul Hoon
authors: CH
authors: Kim
authors: Gi Ho
authors: GH
authors: Seo
authors: Jinu
authors: J
authors: Lee
authors: Joo Hee
authors: JH
authors: Kim
authors: Dong Goo
authors: DG
authors: Kim
authors: Young Soo
authors: YS
authors: Ahn