Effect of 3,4-dihydroxyacetophenone on endothelial dysfunction in streptozotocin-induced rats with type 2 diabetes.

Abstract

This study investigated whether 3,4-Dihydroxyacetophenone (DHAP) could improve endothelial function in streptozotocin-induced type 2 diabetic rats. Sprague-Dawley rats were randomly divided into control, diabetic, and diabetic DHAP-treated animals. After treatment with DHAP for 8 weeks, endothelial function was determined by measuring endothelium-dependent vasodilatation (EDV) of the thoracic aorta. Endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells and nuclear transcription factor kappa B (NF-κB) expression and superoxide anion production in the aorta were determined. DHAP treatment reduced serum levels of triglycerides, cholesterol, malondialdehyde, and tumor necrosis factor α, and enhanced serum adiponectin levels. Endothelium-dependent vasodilatation was significantly attenuated in rats with diabetes and increased significantly after DHAP treatment. NO levels and eNOS activity in endothelial cells were significantly reduced, and NF-κB activation and superoxide production increased in rats with diabetes compared with the control group. DHAP treatment enhanced NO levels and eNOS activity and decreased NF-κB activation and superoxide production. These findings suggest that DHAP could improve endothelial function in streptozotocin-induced type 2 diabetic rats. The mechanism may be related to the enhancement of eNOS activity and NO production by reducing plasma lipid levels, oxidative stress, and inflammatory activity.