Nicotine induces cyclooxygenase-2 and prostaglandin E(2) expression in human umbilical vein endothelial cells.

Nicotine is a major component of cigarette smoking which may be involved in the progress of atherogenesis. In order to explain the mechanism of nicotine-induced endothelium dysfunction, we investigated the effects of nicotine on cyclooxygenase-2 (COX-2) and intercellular adhesion molecule-1 (ICAM-1) expression in human umbilical vein endothelial cells (HUVECs). Nicotine treatment increased the expressions of COX-2 at mRNA and protein level in a dose-dependent manner, following prostaglandin E(2) (PGE(2)) release enhancement. Pyrrolidine dithiocarbamate (PDTC, NF-kappaB inhibitor) and alpha-Bungarotoxin (alpha-Btx, nicotinic acetylcholine receptor antagonist) attenuated the nicotine-induced COX-2 expression and PGE(2) production. Furthermore, nicotine-induced ICAM-1 expression was reduced by NS-398 (selective COX-2 inhibitor). Taken together, the present study demonstrated that nicotine-induced COX-2 expression through NF-kappaB activation which mediated by nicotinic acetylcholine receptor and the induction of COX-2 was related to ICAM-1 expression.