목적: Cigarette smoke is a complex mixture of more than 4700 chemical compounds, including free radicals and highly toxic compounds. Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and airway remodeling in upper airway. Vascular endothelial growth factor (VEGF) is one of the cytokines with a crucial role in tissue remodeling. The aims of this study were to determine the effects of cigarette smoke extract (CSE) on VEGF expression in nasal fibroblasts and to investigate the underlying molecular mechanisms of CSE. 방법:Nasal fibroblasts were stimulated with CSE. Cytotoxicity was evaluated by 3-(4,5- dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Expression level of VEGF was measured using reverse transcription-polymerase chain reaction, and enzyme-linked immunosorbent assay. Activation of reactive oxygen species (ROS) was analyzed by using dichloro-dihydro-fluorescein diacetate assay. Mitogen-activated protein kinase (MAPK) and NF-κB activation were determined by using western blot and/or luciferase assay. 결과:CSE (5%) has no significant cytotoxic effect in nasal fibroblast. CSE significantly increased both VEGF mRNA and protein expression dose-dependently. Pre-treatment of ROS scavengers, p38 inhibitor and NF-kB inhibitor significantly decreased CSE-induced VEGF expression. 결론:CSE has a stimulatory effect on VEGF expression through ROS, p38 and NF-kB signaling pathway in nasal fibroblast.