OBJECTIVES: Reducing the expression of endothelial cell adhesion molecules is conducive to the decrease of inflammation-induced vascular complications. In this study, we observed pitavastatin on expression of vascular cell adhesion molecule-1 (VCAM-1) and its influence on VCAM-1's target gene miR-126 in endothelial cells. The purpose of this study is to explore the mechanism of pitavastatin in prevention and treatment of atherosclerosis. METHODS: HUVEC were cultured in M1640 and passages 2-5 were used in experiments. The cells were randomly divided into three groups, control, TNF-α and pitavastatin group. Cells of TNF-α group were co-incubated with different concentrations (10, 20, 30 μg/L) of TNF-α for 24 h. Cells of pitavastatin group were firstly coincubated with (0.01, 0.1, 1 μmol/L) pitavastatin, respectively, for 1 h, then coincubated with 30 μg/L TNF-α for 24 h. VCAM-1 and miR-126 mRNA were detected by RT-PCR, and Western blotting was used to detect protein expression of VCAM-1. RESULTS: Both detection methods have showed that TNF-α stimulation significantly increased the mRNA and protein expression of VCAM-1 in a dose-dependent manner, and miR-126 mRNA expression exhibited a decreasing trend. The increase of VCAM-1 mRNA and protein expression induced by TNF-α was inhibited by pitavastatin in a dose-dependent manner, too. However, there were no differences of the expression of miR-126 among three groups. CONCLUSIONS: These effects may explain the ability of pitavastatin to reduce the progression of atherosclerosis. The findings further suggest that inhibitory effect of pitavastatin on VCAM-1 is not related to miR-126 but depends on other ways.
OBJECTIVES: Reducing the expression of endothelial cell adhesion molecules is conducive to the decrease of inflammation-induced vascular complications. In this study, we observed pitavastatin on expression of vascular cell adhesion molecule-1 (VCAM-1) and its influence on VCAM-1's target gene miR-126 in endothelial cells. The purpose of this study is to explore the mechanism of pitavastatin in prevention and treatment of atherosclerosis. METHODS: HUVEC were cultured in M1640 and passages 2-5 were used in experiments. The cells were randomly divided into three groups, control, TNF-α and pitavastatin group. Cells of TNF-α group were co-incubated with different concentrations (10, 20, 30 μg/L) of TNF-α for 24 h. Cells of pitavastatin group were firstly coincubated with (0.01, 0.1, 1 μmol/L) pitavastatin, respectively, for 1 h, then coincubated with 30 μg/L TNF-α for 24 h. VCAM-1 and miR-126 mRNA were detected by RT-PCR, and Western blotting was used to detect protein expression of VCAM-1. RESULTS: Both detection methods have showed that TNF-α stimulation significantly increased the mRNA and protein expression of VCAM-1 in a dose-dependent manner, and miR-126 mRNA expression exhibited a decreasing trend. The increase of VCAM-1 mRNA and protein expression induced by TNF-α was inhibited by pitavastatin in a dose-dependent manner, too. However, there were no differences of the expression of miR-126 among three groups. CONCLUSIONS: These effects may explain the ability of pitavastatin to reduce the progression of atherosclerosis. The findings further suggest that inhibitory effect of pitavastatin on VCAM-1 is not related to miR-126 but depends on other ways.