RT Journal Article SR Electronic T1 2′-Hydroxychalcone Inhibits Nuclear Factor-κB and Blocks Tumor Necrosis Factor-α- and Lipopolysaccharide-Induced Adhesion of Neutrophils to Human Umbilical Vein Endothelial Cells JF Molecular Pharmacology JO Mol Pharmacol FD American Society for Pharmacology and Experimental Therapeutics SP 526 OP 534 DO 10.1124/mol.58.3.526 VO 58 IS 3 A1 Babita Madan A1 Sanjay Batra A1 Balaram Ghosh YR 2000 UL http://molpharm.aspetjournals.org/content/58/3/526.abstract AB Inhibition of expression of cell adhesion molecules (CAM), including intercellular CAM-1 (ICAM-1), vascular CAM-1 (VCAM-1), and E-selectin, has been shown to be important in controlling various inflammatory diseases. The cell adhesion proteins are induced by various inflammatory cytokines, such as tumor necrosis factor-α, interleukin-1, and bacterial lipopolysaccharide. The induction process primarily takes place at the level of transcription, where nuclear factor-κB (NF-κB) plays a major role. We demonstrate here that 2′-hydroxychalcone inhibits the adhesion of peripheral neutrophils to the endothelial cell monolayers by inhibiting the expression of ICAM-1, VCAM-1, and E-selectin in a concentration-dependent manner. The inhibition by 2′-hydroxychalcone is reversible. 2′-Hydroxychalcone inhibits the induction of steady-state transcript levels of ICAM-1, VCAM-1, and E-selectin by tumor necrosis factor-α as determined by reverse transcription-polymerase chain reaction, and therefore it may interfere with the transcription of their genes. Because NF-κB is a major transcription factor involved in CAM expression, we studied its status in the 2′-hydroxychalcone treated cells. We demonstrate that 2′-hydroxychalcone inhibits the activation of NF-κB. These results have implications for using NF-κB inhibitors for the treatment of various inflammatory diseases.