Hi, help us enhance your experience
Hi, help us enhance your experience
Hi, help us enhance your experience
291 Views
eMediNexus 01 September 2017
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.
{{Article_Title}}
{{Article_Author}}
{{Article_Title}}
{{Article_Author}}