OBJECTIVETo investigate the effect of rosiglitazone on the expression of nuclear factor-kappaB (NF-kappaB) and coupling factor 6 (CF6) induced by tumor necrosis factor-alpha (TNF-alpha) in cultured human umbilical vein endothelial cells (HUVEC).

METHODSCultured HUVEC of passage 3-5 were stimulated with TNF-alpha and then cultured in the presence of rosiglitazone. The expression of CF6 and NF-kappaB subunit p65 were evaluated by immunocytochemistical method.

RESULTSPretreatment of HUVECs with rosiglitazone inhibited TNF-alpha-induced expression of CF6 in a dose-dependent manner. The activation of CF6 stimulated by TNF-alpha was suppressed by ROS in a dose-dependent manner.

CONCLUSIONTNF-alpha-induced enhancement of the gene expression and release of CF6 is mediated by activation of NF-kappaB signaling pathway. ROS can inhibit the activation of IKK, block NF-kappaB signaling pathway and inhibit the expression of CF6, which may be the mechanism underlying the action of TZDs on hypertension.

Cells, Cultured ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Hypoglycemic Agents ; pharmacology ; Immunohistochemistry ; Mitochondrial Proton-Translocating ATPases ; biosynthesis ; NF-kappa B ; biosynthesis ; Oxidative Phosphorylation Coupling Factors ; biosynthesis ; Thiazolidinediones ; pharmacology ; Tumor Necrosis Factor-alpha ; pharmacology ; Umbilical Veins ; cytology