Chronic or delayed treatment with an oral dithiocarbamate analog decreases glycation and protects diabetic arteries.

In the present study, we examined the efficacy of a dithiocarbamate-based compound, denoted as NOX-700, on diabetes-induced endothelial dysfunction and glycosylation of hemoglobin (Hb). Streptozotocin-induced diabetic rats received 3 mg/ml NOX-700 in drinking water beginning at 72 h or 4 weeks and continued to 8 weeks. Oxidative and glycooxidative stress were examined by electrophoretic mobility shift assay (EMSA) for nuclear factor-kappaB (NF-kappaB) in nuclear fractions of aortic homogenates and by glycosylated Hb, respectively.

Transfection of human endothelial cells with HIV-1 tat gene activates NF-kappa B and enhances monocyte adhesion.

Human immunodeficiency virus (HIV)-1 Tat released from HIV-1-infected monocytes is believed to enter other cells via an integrin-facilitated pathway, resulting in altered gene expression. Indeed, exogenous Tat protein can increase cell adhesion molecule gene expression in human endothelial cells. Signaling pathways initiated by Tat in endothelial cells are not known.

Vascular protective actions of a nitric oxide aspirin analog in both in vitro and in vivo models of diabetes mellitus.

Background: Defective endothelium-dependent relaxation is observed in experimental and human diabetes mellitus. The nature of this defect is not fully understood but may involve decreased nitric oxide (NO) bioactivity due to enhanced production of reactive oxygen species (ROS). In this paper, we examine the benefits and actions of a novel NO-donating, antioxidant called 2-acetoxybenzoic acid 2-(2-nitrooxymethyl) phenyl ester, and denoted as NCX4016, on NO-mediated endothelium-dependent relaxation in normal arteries exposed to acute elevations in glucose or in arteries derived from chronic diabetic animals.