Abstract
Objective To study pitavastatin's effects on nuclear factor-kappa B (NF-κB ) and adhesion molecules in human saphenous vein graft endothelial culture indicating its pleotropic properties. Materials and Method Low-dose (0.1 μM/L) and high-dose (1μM/L) pitavastatin calcium were administered as a frontline therapy in human saphenous endothelial cell culture, followed by induction of inflammation by TNF-α and determination of mRNA level alterations of ICAM-1 and NF-κB genes of endothelial cells using the qRT-PCR method. Additionally, immunofluorescence method was used to show the expression of NF-κB and ICAM-1. Finally, LDH levels were determined by the ELISA method to quantify cytotoxicity. Results ICAM-1 mRNA expression in the low-dose pitavastatin+TNF-α group was significantly higher than that in the TNF-α group and significantly lower than that in the high-dose pitavastatin+TNF-α group (for all comparisons, P = 0.001). The low-dose pitavastatin+TNF-α group had a similar NF-κB mRNA expression with TNF-α and high-dose pitavastatin+TNF-α groups. Conclusion Pitavastatin increases ICAM-1 mRNA expression in saphenous vein endothelial cells. Furthermore, the effect of pitavastatin on adhesion molecules appears independent of NF-κB. Novel studies are needed in this field.
Highlights
In the etiology of atherosclerosis, multiple factors are known to play a role and the pathogenesis of atherosclerosis is known to be extremely complex [1]
In the group treated with 0.1μM pitavastatin, weak immunostaining was observed for intercellular adhesion molecule-1 (ICAM-1)
In the human saphenous vein grafts endothelium pretreated with pitavastatin and stimulated by tumor necrosis factor-α (TNF-α) to form inflammation model, expression of ICAM-1 was increased
Summary
In the etiology of atherosclerosis, multiple factors are known to play a role and the pathogenesis of atherosclerosis is known to be extremely complex [1]. Inflammation plays a predominant role in this complex pathogenesis of atherosclerosis; inflammation takes place in the initiation and the progression of atherosclerosis, and in the development of atherosclerotic complications as acute coronary syndrome [2, 3]. Adhesion molecules have been one of these distinctive candidates with a variety of subtypes [4,5,6,7]. These adhesion molecules, intracellular or intercellular adhesion molecule-1 (ICAM-1) or CD54 (Cluster of Differentiation 54), undertake important functions. ICAM-1 seems to play an important role in the development of atherosclerosis, thrombosis, and inflammation [9, 10]. Nuclear factor-kappa B (NF-κB) is an important transcription factor that has been found to have many functions over the last 30 years
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