casticin and Vasculitis

Pro-inflammatory cytokines induce injury of endothelial cells caused by increases of adhesion molecules, leading to vascular inflammation and the development of atherosclerosis. Recent pharmacological studies have demonstrated that vitexicarpin, a flavonoid isolated from Vitex rotundifolia, has anti-inflammatory, antitumor, and analgesic properties. In this study, we investigated whether vitexicarpin (5-100 nM) prevented the TNF-α-induced vascular inflammation process in human umbilical vein endothelial cells (HUVEC). We found that pretreatment with vitexicarpin decreased TNF-α (10 ng/ml)-induced expression of cell adhesion molecules such as vascular cell adhesion molecule-1, intracellular adhesion molecule-1, and E-selectin as well as matrix metalloproteinase-2 and -9 expression. Preincubation with vitexicarpin also dose-dependently inhibited TNF-α-induced adhesion of HL-60 monocytic cells. Vitexicarpin significantly decreased TNF-α-induced intracellular reactive oxygen species (ROS) production. Furthermore, vitexicarpin suppressed NF-κB nuclear translocation and transcriptional activity in TNF-α-treated HUVEC. In conclusion, vitexicarpin significantly reduced vascular inflammation, through inhibition of ROS-NF-κB pathway in vascular endothelial cells.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Cell Adhesion; Cells, Cultured; E-Selectin; Endothelium, Vascular; Flavonoids; HL-60 Cells; Human Umbilical Vein Endothelial Cells; Humans; Hydrogen Peroxide; Intercellular Adhesion Molecule-1; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; NF-kappa B; Reactive Oxygen Species; Transcription, Genetic; Tumor Necrosis Factor-alpha; Vascular Cell Adhesion Molecule-1; Vasculitis; Vitex