Effect of rosiglitazone on tumor necrosis factor-alpha-induced nuclear factor-kappaB and coupling factor 6 expressions in human umbilical vein endothelial cells.
- Author:
Ze-bing YE
1
;
Zhi-liang LI
;
Shu-dong SONG
;
Di-guang PAN
;
Qiang FU
;
Ying-feng LIU
Author Information
- Publication Type:Journal Article
- MeSH: 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
- From: Journal of Southern Medical University 2008;28(9):1642-1645
- CountryChina
- Language:Chinese
-
Abstract:
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.
