Original ArticleEffect of 3,4-Dihydroxyacetophenone on Endothelial Dysfunction in Streptozotocin-induced Rats With Type 2 DiabetesLiu, Caiyan MD; Sun, Jie MD; Xue, Feng MD; Yi, Yanchun MD; Han, Aiqiang MDAuthor Information Department of Endocrinology, 89th Hospital of Chinese People's Liberation Army, Weifang, China. Reprints: Caiyan Liu, MD, Department of Endocrinology, 89th Hospital of Chinese People's Liberation Army, 256, Beigong West Rd, Weifang 261021, China (e-mail: email@example.com). The authors report no conflicts of interest. Received July 02, 2014 Accepted July 30, 2014 Journal of Cardiovascular Pharmacology: January 2015 - Volume 65 - Issue 1 - p 22-27 doi: 10.1097/FJC.0000000000000158 Buy Metrics Abstract 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. © 2015 by Lippincott Williams & Wilkins.