Abstract

Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are important adhesion molecules. The present study was undertaken to observe effects of atorvastatin (ATV) on mRNA and protein expression of ICAM-1 and VCAM-1 in cultured human umbilical vein endothelial cells activated by tumor necrosis factor (TNF)-α and interleukin (IL)-1β. The levels of mRNA (detected by RT-PCR) and protein (measured by Western blot) of ICAM-1 and VCAM-1 increased initially after cells were coincubated with 10μg/L TNF-α and IL-1β (P<0.01), and reached peak with 30μg/L TNF-α and IL-1β; With 30μg/L TNF-α and IL-1β, mRNA and protein of ICAM-1 and VCAM-1 increased from 0h to 48h (P<0.01), and maintained high level until 72h. Compared with control, ICAM-1 mRNA of TNF-α, IL-1β and ATV (10, 1.0, 0.1μmol/L) groups induced 2.23-fold, 2.42-fold,1.02-fold (*P<0.05 vs TNF-α or IL-1β group), 1.36- fold* and 1.12-fold* increases, respectively. Compared with control, VCAM-1 mRNA of TNF-α, IL-1β and ATV (10, 1.0, 0.1 μmol/L) groups induced 2.35-fold, 2.41-fold, 1.10-fold (*P<0.05 vs TNF-α or IL-1β group), 1.28-fold* and 1.33-fold* increases, respectively. The protein of ICAM-1 and VCAM-1 of TNF-α and IL-1β groups were higher than control (P<0.01), and ATV reduced (P<0.05) the increases in the protein of ICAM-1 and VCAM-1 induced by TNF-α and IL-1β. TNF-α and IL-1β dose-dependently and time-dependently induced increases in the mRNA and protein of ICAM-1 and VCAM-1, and ATV dose-dependently reduced (P<0.05) the increases in the mRNA and protein of ICAM-1 and VCAM-1 induced by TNF-α and IL-1β. The results suggest that ATV increases the stability of plaques and slows down the progression of atherosclerosis.

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