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Rosuvastatin inhibits high glucose-stimulated upregulation of VCAM-1 via the MAPK-signalling pathway in endothelial cells.
Acta Cardiologica 2018 Februrary
OBJECTIVE: The aim of this study is to investigate the molecular mechanisms and effect of rosuvastatin on adhesion molecule induction in human endothelial cells under high-glucose conditions (HG).
METHODS AND RESULTS: The effects of rosuvastatin on vascular cell adhesion molecule (VCAM)-1 production and pERK phosphorylation were measured in HG-induced human umbilical vein endothelial cells (HUVECs) with inhibitors targeting the mitogen-activated protein kinase (MAPK) signal pathway. HG increased levels of VCAM-1. Treatment with rosuvastatin inhibited VCAM-1 expression in a concentration- and time-dependent manner. In addition, we investigated the effects of rosuvastatin on the extracellular signal-regulated kinase (ERK) 1/2 signal pathway. Rosuvastatin completely inhibited HG-induced phosphorylation of ERK. ERK/MAPK inhibitors completely prevented the VCAM-1 inhibition effect of rosuvastatin under HG condition.
CONCLUSIONS: This study demonstrated that rosuvastatin suppresses HG-induced VCAM-1 production via the MAPK signalling pathway, playing a role in the suppression of atherosclerosis.
METHODS AND RESULTS: The effects of rosuvastatin on vascular cell adhesion molecule (VCAM)-1 production and pERK phosphorylation were measured in HG-induced human umbilical vein endothelial cells (HUVECs) with inhibitors targeting the mitogen-activated protein kinase (MAPK) signal pathway. HG increased levels of VCAM-1. Treatment with rosuvastatin inhibited VCAM-1 expression in a concentration- and time-dependent manner. In addition, we investigated the effects of rosuvastatin on the extracellular signal-regulated kinase (ERK) 1/2 signal pathway. Rosuvastatin completely inhibited HG-induced phosphorylation of ERK. ERK/MAPK inhibitors completely prevented the VCAM-1 inhibition effect of rosuvastatin under HG condition.
CONCLUSIONS: This study demonstrated that rosuvastatin suppresses HG-induced VCAM-1 production via the MAPK signalling pathway, playing a role in the suppression of atherosclerosis.
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