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-Lipoic acid inhibits TNF--induced NF-
B activation and adhesion molecule expression in human aortic endothelial cells
Linus Pauling Institute, Oregon State University, Corvallis, Oregon 97331, USA
1Correspondence: Linus Pauling Institute, Oregon State University, 571 Weniger Hall, Corvallis, OR 97331, USA. E-mail: Balz.frei{at}orst.edu
Endothelial activation and monocyte adhesion are initiating steps in atherogenesis thought to be caused in part by oxidative stress. The metabolic thiol antioxidant 
-lipoic acid has been suggested to be of therapeutic value in pathologies associated with redox imbalances. We investigated the role of (R)--lipoic acid (LA) vs. glutathione and ascorbic acid in tumor necrosis factor (TNF-) -induced adhesion molecule expression and nuclear factor 
B (NF-B) signaling in human aortic endothelial cells (HAEC). Preincubation of HAEC for 48 h with LA (0.05–1 mmol/l) dose-dependently inhibited TNF- (10 U/ml) -induced adhesion of human monocytic THP-1 cells, as well as mRNA and protein expression of E-selectin, vascular cell adhesion molecule 1 and intercellular adhesion molecule 1. LA also strongly inhibited TNF--induced mRNA expression of monocyte chemoattractant protein-1 but did not affect expression of TNF- receptor 1. Furthermore, LA dose-dependently inhibited TNF--induced IB kinase activation, subsequent degradation of IB, the cytoplasmic NF-B inhibitor, and nuclear translocation of NF-B. In contrast, TNF--induced NF-B activation and adhesion molecule expression were not affected by ascorbic acid or by manipulating cellular glutathione status with L-2-oxo-4-thiazolidinecarboxylic acid, N-acetyl-L-cysteine, or D,L-buthionine-S,R-sulfoximine. Our data show that clinically relevant concentrations of LA, but neither vitamin C nor glutathione, inhibit adhesion molecule expression in HAEC and monocyte adhesion by inhibiting the IB/NF-B signaling pathway at the level, or upstream, of IB kinase.—Zhang, W.-J., Frei, B. -Lipoic acid inhibits TNF--induced NF-B activation and adhesion molecule expression in human aortic endothelial cells.
Key Words: antioxidants • adhesion molecules • endothelium • nuclear factor B
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