Abstract
Dihydromyricetin (DHY), a flavonoid component isolated from Ampelopsis grossedentata, exerts versatile pharmacological activities. However, the possible effects of DHY on diabetic vascular endothelial dysfunction have not yet been fully elucidated. In the present study, male C57BL/6 mice, wild type (WT) 129S1/SvImJ mice and sirtuin 3 (SIRT3) knockout (SIRT3-/-) mice were injected with streptozotocin (STZ, 60 mg/kg/day) for 5 consecutive days. Two weeks later, DHY were given at the doses of 250 mg/kg by gavage once daily for 12 weeks. Fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) level, endothelium-dependent relaxation of thoracic aorta, reactive oxygen species (ROS) production, SIRT3, and superoxide dismutase 2 (SOD2) protein expressions, as well as mitochondrial Deoxyribonucleic Acid (mtDNA) copy number, in thoracic aorta were detected. Our study found that DHY treatment decreased FBG and HbA1c level, improved endothelium-dependent relaxation of thoracic aorta, inhibited oxidative stress and ROS production, and enhanced SIRT3 and SOD2 protein expression, as well as mtDNA copy number, in thoracic aorta of diabetic mice. However, above protective effects of DHY were unavailable in SIRT3-/- mice. The study suggested DHY improved endothelial dysfunction in diabetic mice via oxidative stress inhibition in a SIRT3-dependent manner.
Highlights
Diabetes is a chronic disease characterized by hyperglycemia
It is noting that a marked increase in HbA1c level compared to mice in the control group
It is noting that therethere was was significant decline in Fasting blood glucose (FBG)
Summary
Diabetes is a chronic disease characterized by hyperglycemia. The increasing prevalence of diabetes becomes a serious global health problem [1,2,3]. There are various chronic complications of diabetes, which are the main cause of morbidity and mortality of diabetes, including: diabetic nephropathy, neuropathy, retinopathy, lower extremity vascular lesions, and gastroenteropathy [4,5,6,7]. Prolonged hyperglycemia may impair endothelial function of macro- and micro-vascular to increase risks for cardiovascular disease in diabetes [8,9]. It is of great importance to improve endothelial function in diabetes. The detailed molecular mechanisms involved in endothelial dysfunction with diabetes are complex. Oxidative stress is considered to be one key factor causing diabetic vascular endothelial dysfunction [10,11,12,13].
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