Catechol, a Bioactive Degradation Product of Salicortin, Reduces TNF-α Induced ICAM-1 Expression in Human Endothelial Cells

The phenolic glucoside salicortin was isolated from a Willow bark extract, and its ability to reduce the TNF-alpha induced ICAM-1 expression (10 ng/mL, 30 min pretreatment with salicortin) was tested in vitro on human microvascular endothelial cells (HMEC-1). After 24 h, 25 mu M salicortin decreased the TNF-a induced ICAM-1 expression to 65.9% compared to cells which were treated only with TNF-a. In parallel, the stability of 25 mu M salicortin under assay conditions was determined by HPLC. Within 24 h, the salicortin concentration decreased to 3.1 mu M whereas catechol, a known NF-kappa B inhibitor, rose as a metabolite. After 8 h the catechol concentration was relatively constant and varied between 8.2 and 10.9 mu M. Considering this degradation in the in vitro test system, 10 mu M catechol was added 8 h after TNF-a stimulation, and 16 h later the ICAM-1 expression was determined. In this setting, the ICAM-1 expression was reduced to 74.8%. This is comparable to the effect obtained from 25 mu M salicortin and indicates that its activity is related to the generation of catechol, as salicin, saligenin, and salicylic acid are only marginally active or inactive in this test system in a concentration up to 50 mu M. These results indicate catechol as an important bioactive metabolite from salicortin.