In this study, 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.

A new study published in the Acta Cardiologica investigated the molecular mechanisms and effect of rosuvastatin on adhesion molecule induction in human endothelial cells under high-glucose conditions (HG). In this study, 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. Additionally, the effects of rosuvastatin on the extracellular signal-regulated kinase (ERK) 1/2 signal pathway were examined. It was observed that HG increased levels of VCAM-1. Whereas, treatment with rosuvastatin inhibited VCAM-1 expression in a concentration- and time-dependent manner. Furthermore, rosuvastatin completely inhibited HG-induced phosphorylation of ERK. ERK/MAPK inhibitors completely prevented the VCAM-1 inhibition effect of rosuvastatin under HG condition. The findings of this study indicated that rosuvastatin suppresses HG-induced VCAM-1 production via MAPK signaling pathway and plays a role in the suppression of atherosclerosis.