XXXX Reduces Endothelium Dysfunction through the PKG-I Pathway.

@entity6708 @entity1 @entity42614 @entity35777 @entity2806 @entity63 @entity51180 @entity519 @entity35 @entity73303
Purpose. In this report, we investigated the protective mechanism of @entity42614 ( @entity35777 ) in vitro and in vivo which could be involved in endothelial @entity6708 -dependent protein kinase (PKG), @entity51180 ( @entity51180 ) pathway, and vascular endothelium dysfunction (EtD). Method. @entity1 brain microvascular endothelial cells (HBMECs) with @entity519 reoxygenation (HR) treatment and @entity35 with @entity2806 reperfusion (CIR) treatment were applied. Protein and mRNA expression of PKG, @entity51180 , and p- @entity51180 were evaluated by Western blot and RT-PCR methods. Vascular EtD was assessed by using wire myography to determine endothelium-dependent vasorelaxation in isolated @entity35 basilar artery (BA). Result. In cultured HBMECs, @entity35777 (0.1, 1, and 10    M) increased cell viability, mRNA, protein level, and phosphorylative activity of PKG and @entity51180 against @entity519 . In HR model of BA, @entity35777 increased protein level of P- @entity51180 . In @entity35 CIR model, wire myography demonstrated that @entity35777 (45 and 90   mg/kg, i.v.) significantly reduced @entity63 size by partially restoring the endothelium dependent vasodilation of BA; PKG inhibitor @entity73303 (50    g/kg, i.v.) reversed this protection of @entity35777 in CIR @entity35 . Conclusion. @entity35777 protects against cerebral vascular EtD through endothelial PKG pathway activation.
