Genipin Selectively Inhibits TNF-alpha-activated VCAM-1 But Not ICAM-1 Expression by Upregulation of PPAR-gamma in Human Endothelial Cells
The Korean Journal of Physiology and Pharmacology
;
: 157-162, 2011.
Artigo
em Inglês
| WPRIM
| ID: wpr-727887
ABSTRACT
Vascular inflammation process has been suggested to be an important risk factor in the development of atherosclerosis. Recently we reported that induction of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) selectively inhibits vascular cell adhesion molecule-1 (VCAM-1) but not intercellular cell adhesion molecule-1 (ICAM-1) in tumor necrosis factor (TNF)-alpha-activated human umbilical vein endothelial cells (HUVEC). In this study, we investigated whether genipin inhibits expression of cellular adhesion molecules, which is relevant to inflammation. Pretreatment with genipin reduced reactive oxygen species (ROS) production and expression of VCAM-1, but not ICAM-1 in TNF-alpha-activated HUVEC. Genipin dose- and time-dependently increased PPAR-gamma expression and inhibited TNF-alpha-induced phosphorylation of Akt and PKC with different degrees. Finally, genipin prevented TNF-alpha-induced adhesion of U937 monocytic cells to HUVEC. Taken together, these results indicate that upregualtion of PPAR-gamma by genipin selectively inhibits TNF-alpha-induced expression of VCAM-1, in which regulation of Akt and/or PKC play a key role. We concluded that genipin can be used for the treatment of cardiovascular disorders such as atherosclerosis.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosforilação
/
Adesão Celular
/
Regulação para Cima
/
Fatores de Risco
/
Fator de Necrose Tumoral alfa
/
Espécies Reativas de Oxigênio
/
Molécula 1 de Adesão Intercelular
/
Molécula 1 de Adesão de Célula Vascular
/
Peroxissomos
/
Iridoides
Tipo de estudo:
Estudo de etiologia
/
Fatores de risco
Limite:
Humanos
Idioma:
Inglês
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
2011
Tipo de documento:
Artigo
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